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18 Harvey V Sparks M D CHAPTER Control Mechanisms in

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completes a negative-feedback loop by which increases in mean arterial pressure can be attenuated. Conversely, decreases in arterial pressure (and decreased stretch of the baroreceptors) increase sympathetic neural activity and decrease parasympathetic neural activity, re-sulting in increased heart rate, stroke volume, and SVR; this

CHAPTER 18 Control Mechanisms in Circulatory Function 291
AUTONOMIC NEURAL CONTROL OF THE thetic nervous system activity parasympathetic activation
CIRCULATORY SYSTEM reduces cardiac contractility
Sympathetic fibers to the heart release NE which binds
Neural regulation of the cardiovascular system involves the to 1 adrenergic receptors in the sinoatrial node the atri
firing of postganglionic parasympathetic and sympathetic oventricular node and specialized conducting tissues and
neurons triggered by preganglionic neurons in the brain cardiac muscle Stimulation of these fibers causes increased
parasympathetic and spinal cord sympathetic and heart rate conduction velocity and contractility
parasympathetic Afferent input influencing these neurons The two divisions of the autonomic nervous system tend
comes from the cardiovascular system as well as from other to oppose each other in their effects on the heart and ac
organs and the external environment tivities along these two pathways usually change in a recip
Autonomic control of the heart and blood vessels was rocal manner
described in Chapter 6 Briefly the heart is innervated by Blood vessels except those of the external genitalia re
parasympathetic vagus and sympathetic cardioaccelera ceive sympathetic innervation only see Fig 18 1 The
tor nerve fibers Fig 18 1 Parasympathetic fibers release neurotransmitter is NE which binds to 1 adrenergic re
acetylcholine ACh which binds to muscarinic receptors ceptors and causes vascular smooth muscle contraction and
of the sinoatrial node the atrioventricular node and spe vasoconstriction Circulating epinephrine released from
cialized conducting tissues Stimulation of parasympathetic the adrenal medulla binds to 2 adrenergic receptors of
fibers causes a slowing of the heart rate and conduction ve vascular smooth muscle cells especially coronary and
locity The ventricles are only sparsely innervated by skeletal muscle arterioles producing vascular smooth mus
parasympathetic nerve fibers and stimulation of these cle relaxation and vasodilation Postganglionic parasympa
fibers has little direct effect on cardiac contractility Some thetic fibers release ACh and nitric oxide NO to blood
cardiac parasympathetic fibers end on sympathetic nerves vessels in the external genitalia ACh causes the further re
and inhibit the release of norepinephrine NE from sym lease of NO from endothelial cells NO results in vascular
pathetic nerve fibers Therefore in the presence of sympa smooth muscle relaxation and vasodilation
Parasympathetic Sympathetic
medulla ACh
Most blood
Sacral Blood vessels
of external
FIGURE 18 1 Autonomic innervation of the cardiovascular system ACh acetylcholine NE norepi
nephrine E epinephrine SA sinoatrial node AV atrioventricular node
The Spinal Cord Exerts Control Over Changes in the firing rate of the arterial baroreceptors
Cardiovascular Function and cardiopulmonary baroreceptors initiate reflex re
sponses of the autonomic nervous system that alter cardiac
Preganglionic sympathetic neurons normally generate a output and SVR The central terminals for these receptors
steady level of background postganglionic activity tone are located in the nucleus tractus solitarii NTS in the
This sympathetic tone produces a background level of medulla oblongata Neurons from the NTS project to the
sympathetic vasoconstriction cardiac stimulation and RVL and nucleus ambiguus where they influence the firing
adrenal medullary catecholamine secretion all of which of sympathetic and parasympathetic nerves
contribute to the maintenance of normal blood pressure
This tonic activity is generated by excitatory signals from
Baroreceptor Reflex Effects on Cardiac Output and Sys
the medulla oblongata When the spinal cord is acutely
temic Vascular Resistance Increased pressure in the
transected and these excitatory signals can no longer
carotid sinus and aorta stretches carotid sinus barorecep
reach sympathetic preganglionic fibers their tonic firing
tors and aortic baroreceptors and raises their firing rate
is reduced and blood pressure falls an effect known as
Nerve fibers from carotid sinus baroreceptors join the glos
spinal shock
sopharyngeal cranial nerve IX nerves and travel to the
Humans have spinal reflexes of cardiovascular signifi
NTS Nerve fibers from the aortic baroreceptors located in
cance For example the stimulation of pain fibers entering
the wall of the arch of the aorta travel with the vagus cra
the spinal cord below the level of a chronic spinal cord
nial nerve X nerves to the NTS
transection can cause reflex vasoconstriction and increased
The increased action potential traffic reaching the NTS
blood pressure
leads to excitation of nucleus ambiguus neurons and inhibi
tion of firing of RVL neurons This results in increased
The Medulla Is a Major Area for Cardiovascular parasympathetic neural activity to the heart and decreased
Reflex Integration sympathetic neural activity to the heart and resistance ves
sels primarily arterioles Fig 18 2 causing decreased car
The medulla oblongata has three major cardiovascular diac output and SVR Since mean arterial pressure is the
functions product of SVR and cardiac output see Chapter 12 mean
Generating tonic excitatory signals to spinal sympa arterial pressure is returned toward the normal level This
thetic preganglionic fibers completes a negative feedback loop by which increases in
Integrating cardiovascular reflexes mean arterial pressure can be attenuated
Integrating signals from supramedullary neural networks Conversely decreases in arterial pressure and decreased
and from circulating hormones and drugs stretch of the baroreceptors increase sympathetic neural
Specific pools of neurons are responsible for elements of activity and decrease parasympathetic neural activity re
these functions Neurons in the rostral ventrolateral nu sulting in increased heart rate stroke volume and SVR this
cleus RVL are normally active and provide tonic excita
tory activity to the spinal cord Specific pools of neurons
within the RVL have actions on heart and blood vessels
RVL neurons are critical in mediating reflex inhibition or
activating sympathetic firing to the heart and blood vessels
The cell bodies of cardiac preganglionic parasympathetic
neurons are located in the nucleus ambiguus the activity
of these neurons is influenced by reflex input as well as in
put from respiratory neurons Respiratory sinus arrhythmia
described in Chapter 13 is primarily the result of the influ
ence of medullary respiratory neurons that inhibit firing of
preganglionic parasympathetic neurons during inspiration
and excite these neurons during expiration Other inputs to
the RVL and nucleus ambiguus will be described below
The Baroreceptor Reflex Is Important in the
Regulation of Arterial Pressure
The most important reflex behavior of the cardiovascular
system originates in mechanoreceptors located in the aorta
carotid sinuses atria ventricles and pulmonary vessels
These mechanoreceptors are sensitive to the stretch of the
walls of these structures When the wall is stretched by in
Baroreceptor reflex response to increased
creased transmural pressure receptor firing rate increases FIGURE 18 2
arterial pressure An intervention elevates ar
Mechanoreceptors in the aorta and carotid sinuses are terial pressure either mean arterial pressure or pulse pressure
called baroreceptors Mechanoreceptors in the atria ven stretches the baroreceptors and initiates the reflex The resulting
tricles and pulmonary vessels are referred to as low pres reduced systemic vascular resistance and cardiac output return ar
sure baroreceptors or cardiopulmonary baroreceptors terial pressure toward the level existing before the intervention
CHAPTER 18 Control Mechanisms in Circulatory Function 293
returns blood pressure toward the normal level If the fall in
mean arterial pressure is very large increased sympathetic
neural activity to veins is added to the above responses
causing contraction of the venous smooth muscle and re
ducing venous compliance Decreased venous compliance
shifts blood toward the central blood volume increasing
right atrial pressure and in turn stroke volume
Baroreceptor Reflex Effects on Hormone Levels The
baroreceptor reflex influences hormone levels in addition
to vascular and cardiac muscle The most important influ
ence is on the renin angiotensin aldosterone system
RAAS A reduction in arterial pressure and baroreceptor
firing results in increased sympathetic nerve activity to the
kidneys which causes the kidneys to release renin activat
ing the RAAS The activation of this system causes the kid
neys to save salt and water Salt and water retention in
creases blood volume and ultimately causes blood
pressure to rise The details of the RAAS are discussed later
in this chapter and in Chapter 24
The information on the firing rate of the baroreceptors Carotid sinus baroreceptor nerve firing rate
is also projected to the paraventricular nucleus of the hy and mean arterial pressure With normal
pothalamus where the release of arginine vasopressin conditions a mean arterial pressure of 93 mm Hg is near the
AVP by the posterior pituitary is controlled see Chapter midrange of the firing rates for the nerves Sustained hyperten
32 Decreased firing rate of the baroreceptors results in in sion causes the operating range to shift to the right putting 93
creased AVP release causing the kidney to save water The mm Hg at the lower end of the firing range for the nerves
result is an increase in blood volume An increase in arterial
pressure causes decreased AVP release and increased excre
tion of water by the kidneys mately 40 mm Hg when the receptor stops firing to 180
Hormonal effects on salt and water balance and ulti mm Hg when the firing rate reaches a maximum
mately on cardiac output and blood pressure are powerful Fig 18 3 Pulse pressure also influences the firing rate of the
but they occur more slowly a timescale of many hours to baroreceptors For a given mean arterial pressure the firing
days than ANS effects seconds to minutes rate of the baroreceptors increases with pulse pressure
Baroreceptor Reflex Effects on Specific Organs The Baroreceptor Adaptation An important property of the
defense of arterial pressure by the baroreceptor reflex re baroreceptor reflex is that it adapts during a period of 1 to
sults in maintenance of blood flow to two vital organs the 2 days to the prevailing mean arterial pressure When the
heart and brain If resistance vessels of the heart and brain mean arterial pressure is suddenly raised baroreceptor fir
participated in the sympathetically mediated vasoconstric ing increases If arterial pressure is held at the higher level
tion found in skeletal muscle skin and the splanchnic re baroreceptor firing declines during the next few seconds
gion it would lower blood flow to these organs This does Firing rate then continues to decline more slowly until it re
not happen turns to the original firing rate between 1 and 2 days Con
The combination of 1 a minimal vasoconstrictor effect sequently if the mean arterial pressure is maintained at an
of sympathetic nerves on cerebral blood vessels and 2 a elevated level the tendency for the baroreceptors to initi
robust autoregulatory response keeps brain blood flow ate a decrease in cardiac output and SVR quickly disap
nearly normal despite modest decreases in arterial pressure pears This occurs in part because of the reduction in the
see Chapter 17 However a large decrease in arterial rate of baroreceptor firing for a given mean arterial pressure
pressure beyond the autoregulatory range causes brain mentioned above see Fig 18 3 This is an example of re
blood flow to fall accounting for loss of consciousness ceptor adaptation A resetting of the reflex in the central
Activation of sympathetic nerves to the heart causes 1 nervous system CNS occurs as well Consequently the
adrenergic receptor mediated constriction of coronary ar baroreceptor mechanism is the first line of defense in the
terioles and 1 adrenergic receptor mediated increases in maintenance of normal blood pressure it makes the rapid
cardiac muscle metabolism see Chapter 17 The net effect control of blood pressure needed with changes in posture
is a marked increase in coronary blood flow despite the in or blood loss possible but it does not provide for the long
creased sympathetic constrictor activity In summary when term control of blood pressure
arterial pressure drops the generalized vasoconstriction
caused by the baroreflex spares the brain and heart allow Cardiopulmonary Baroreceptors Are Stretch
ing flow to these two vital organs to be maintained
Receptors That Sense Central Blood Volume
Pressure Range for Baroreceptors The effective range Cardiopulmonary baroreceptors are located in the cardiac
of the carotid sinus baroreceptor mechanism is approxi atria at the junction of the great veins and atria in the ven
tricular myocardium and in pulmonary vessels Their nerve creased parasympathetic activity to the heart These events
fibers run in the vagus nerve to the NTS with projections lead to increases in cardiac output SVR and mean arterial
to supramedullary areas as well Unloading i e decreasing pressure An example of this reaction is the cold pressor re
the stretch of the cardiopulmonary receptors by reducing sponse the elevated blood pressure that normally occurs
central blood volume results in increased sympathetic when an extremity is placed in ice water The increase in
nerve activity and decreased parasympathetic nerve activ blood pressure produced by this challenge is exaggerated in
ity to the heart and blood vessels In addition the car several forms of hypertension
diopulmonary reflex interacts with the baroreceptor reflex A second type of response is produced by deep pain
Unloading of the cardiopulmonary receptors enhances the The stimulation of deep pain fibers associated with crush
baroreceptor reflex and loading the cardiopulmonary re ing injuries disruption of joints testicular trauma or dis
ceptors by increasing central blood volume inhibits the tension of the abdominal organs results in diminished sym
baroreceptor reflex pathetic activity and enhanced parasympathetic activity
Like the arterial baroreceptors the decreased stretch of with decreased cardiac output SVR and blood pressure
the cardiopulmonary baroreceptors activates the RAAS and This hypotensive response contributes to certain forms of
increases the release of AVP cardiovascular shock
Chemoreceptors Detect Changes Activation of Chemoreceptors in the
in PCO2 pH and PO2 Ventricular Myocardium Causes Reflex
Bradycardia and Vasodilation
The reflex response to changes in blood gases and pH be
gins with chemoreceptors located peripherally in the An injection of bradykinin 5 hydroxytryptamine sero
carotid bodies and aortic bodies and centrally in the tonin certain prostaglandins or various other compounds
medulla see Chapter 22 The peripheral chemoreceptors into the coronary arteries supplying the posterior and inferior
of the carotid bodies and aortic bodies are specialized regions of the ventricles causes reflex bradycardia and hy
structures located in approximately the same areas as the potension The chemoreceptor afferents are carried in the va
carotid sinus and aortic baroreceptors They send nerve im gus nerves The bradycardia results from increased parasym
pulses to the NTS and are sensitive to elevated PCO2 as pathetic tone Dilation of systemic arterioles and veins is
well as decreased pH and PO2 Peripheral chemoreceptors caused by withdrawal of sympathetic tone This reflex is also
exhibit an increased firing rate when 1 the PO2 or pH of elicited by myocardial ischemia and is responsible for the
the arterial blood is low 2 the PCO2 of arterial blood is in bradycardia and hypotension that can occur in response to
creased 3 the flow through the bodies is very low or acute infarction of the posterior or inferior myocardium
stopped or 4 a chemical is given that blocks oxidative
metabolism in the chemoreceptor cells The central
medullary chemoreceptors increase their firing rate prima INTEGRATED SUPRAMEDULLARY
rily in response to elevated arterial PCO2 which causes a CARDIOVASCULAR CONTROL
decrease in brain pH
The increased firing of both peripheral and central The highest levels of organization in the ANS are the
chemoreceptors via the NTS and RVL leads to profound supramedullary networks of neurons with way stations in
peripheral vasoconstriction Arterial pressure is signifi the limbic cortex amygdala and hypothalamus These
cantly elevated If respiratory movements are voluntarily supramedullary networks orchestrate cardiovascular corre
stopped the vasoconstriction is more intense and a striking lates of specific patterns of emotion and behavior by their
bradycardia and decreased cardiac output occur This re projections to the ANS
sponse pattern is typical of the diving response discussed Unlike the medulla supramedullary networks do not
later As in the case of the baroreceptor reflex the coro contribute to the tonic maintenance of blood pressure nor
nary and cerebral circulations are not subject to the sympa are they necessary for most cardiovascular reflexes al
thetic vasoconstrictor effects and instead exhibit vasodila though they modulate reflex reactivity
tion as a result of the combination of the direct effect of
the abnormal blood gases and local metabolic effects
In addition to its importance when arterial blood gases The Fight or Flight Response Includes
are abnormal the chemoreceptor reflex is important in the Specific Cardiovascular Changes
cardiovascular response to severe hypotension As blood Upon stimulation of certain areas in the hypothalamus cats
pressure falls blood flow through the carotid and aortic demonstrate a stereotypical rage response with spitting
bodies decreases and chemoreceptor firing increases clawing tail lashing back arching and so on This is ac
probably because of changes in local PCO2 pH and PO2 companied by the autonomic fight or flight response de
scribed in Chapter 6 Cardiovascular responses include ele
Pain Receptors Produce Reflex Responses vated heart rate and blood pressure
The initial behavioral pattern during the fight or flight
in the Cardiovascular System
response includes increased skeletal muscle tone and gen
Two reflex cardiovascular responses to pain occur In the eral alertness There is increased sympathetic neural activ
most common reflex pain causes increased sympathetic ac ity to blood vessels and the heart The result of this cardio
tivity to the heart and blood vessels coupled with de vascular response is an increase in cardiac output by
CHAPTER 18 Control Mechanisms in Circulatory Function 295
increasing both heart rate and stroke volume SVR and ar and peripheral vasoconstriction sympathetic of the ex
terial pressure When the fight or flight response is con tremities and splanchnic regions when his or her face is
summated by fight or flight arterioles in skeletal muscle di submerged in cold water With breath holding during the
late because of accumulation of local metabolites from the dive arterial PO2 and pH fall and PCO2 rises and the
exercising muscles see Chapter 17 This vasodilation may chemoreceptor reflex reinforces the diving response The
outweigh the sympathetic vasoconstriction in other organs arterioles of the brain and heart do not constrict and there
and SVR may actually fall With a fall in SVR mean arterial fore cardiac output is distributed to these organs This
pressure returns toward normal despite the increase in car heart brain circuit makes use of the oxygen stored in the
diac output blood that would normally be used by the other tissues es
Emotional situations often provoke the fight or flight pecially skeletal muscle Once the diver surfaces the heart
response in humans but it is usually not accompanied by rate and cardiac output increase substantially peripheral
muscle exercise e g medical students taking an examina vasoconstriction is replaced by vasodilation restoring nu
tion It seems likely that repeated elevations in arterial trient flow and washing out accumulated waste products
pressure caused by dissociation of the cardiovascular com
ponent of the fight or flight response from muscular exer
cise component are harmful Behavioral Conditioning Affects
Cardiovascular Responses
Fainting Can Be a Cardiovascular Cardiovascular responses can be conditioned as can other
Correlate of Emotion autonomic responses such as those observed in Pavlov s fa
mous experiments Both classical and operant condition
Vasovagal syncope fainting is a somatic and cardiovascu ing techniques have been used to raise and lower the blood
lar response to certain emotional experiences Stimulation pressure and heart rate of animals Humans can also be
of specific areas of the cerebral cortex can lead to a sudden taught to alter their heart rate and blood pressure using a
relaxation of skeletal muscles depression of respiration variety of behavioral techniques such as biofeedback
and loss of consciousness The cardiovascular events ac Behavioral conditioning of cardiovascular responses has
companying these somatic changes include profound significant clinical implications Animal and human studies
parasympathetic induced bradycardia and withdrawal of indicate that psychological stress can raise blood pressure
resting sympathetic vasoconstrictor tone There is a dra increase atherogenesis and predispose to fatal cardiac ar
matic drop in heart rate cardiac output and SVR The re rhythmias These effects are thought to result from an in
sultant decrease in mean arterial pressure results in uncon appropriate fight or flight response Other studies have
sciousness because of lowered cerebral blood flow shown beneficial effects of behavior patterns designed to
Vasovagal syncope appears in lower animals as the playing introduce a sense of relaxation and well being Some clini
dead response typical of the opossum cal regimens for the treatment of cardiovascular disease
take these factors into account
The Cardiovascular Correlates of Exercise Require
Integration of Central and Peripheral Mechanisms Not All Cardiovascular Responses Are Equal
Exercise causes activation of supramedullary neural net Supramedullary responses can override the baroreceptor re
works that inhibit the activity of the baroreceptor reflex flex For example the fight or flight response causes the
The inhibition of medullary regions involved in the barore heart rate to rise above normal levels despite a simultaneous
ceptor reflex is called central command Central command rise in arterial pressure In such circumstances the neurons
results in withdrawal of parasympathetic tone to the heart connecting the hypothalamus to medullary areas inhibit the
with a resulting increase in heart rate and cardiac output baroreceptor reflex and allow the corticohypothalamic re
The increased cardiac output supplies the added require sponse to predominate Also during exercise input from
ment for blood flow to exercising muscle As exercise in supramedullary regions inhibits the baroreceptor reflex pro
tensity increases central command adds sympathetic tone moting increased sympathetic tone and decreased parasym
that further increases heart rate and contractility It also re pathetic tone despite an increase in arterial pressure
cruits sympathetic vasoconstriction that redistributes blood Moreover the various cardiovascular response patterns
flow away from splanchnic organs and resting skeletal mus do not necessarily occur in isolation as previously de
cle to exercising muscle Finally afferent impulses from ex scribed Many response patterns interact reflecting the ex
ercising skeletal muscle terminate in the RVL where they tensive neural interconnections between all levels of the
further augment sympathetic tone CNS and interaction with various elements of the local
During exercise blood flow of the skin is largely influ control systems For example the baroreceptor reflex inter
enced by temperature regulation as described in Chapter 17 acts with thermoregulatory responses Cutaneous sympa
thetic nerves participate in body temperature regulation
The Diving Response Maintains Oxygen see Chapter 29 but also serve the baroreceptor reflex At
Delivery to the Heart and Brain moderate levels of heat stress the baroreceptor reflex can
cause cutaneous arteriolar constriction despite elevated
The diving response is best observed in seals and ducks core temperature However with severe heat stress the
but it also occurs in humans An experienced diver can ex baroreceptor reflex cannot overcome the cutaneous vasodi
hibit intense slowing of the heart rate parasympathetic lation as a result arterial pressure regulation may fail
HORMONAL CONTROL OF THE temic vasoconstriction and increases mean arterial pressure
CARDIOVASCULAR SYSTEM The reflex masks some of the direct cardiac effects of NE by
significantly increasing cardiac parasympathetic tone In
Various hormones play a role in the control of the cardio contrast epinephrine causes vasodilation in skeletal muscle
vascular system Important sites of hormone secretion in and splanchnic beds SVR may actually fall and mean arte
clude the adrenal medulla posterior pituitary gland kid rial pressure does not rise The baroreceptor reflex is not
ney and cardiac atrium elicited parasympathetic tone to the heart is not increased
and the direct cardiac effects of epinephrine are evident At
Circulating Epinephrine Has high concentrations epinephrine binds to 1 adrenergic
Cardiovascular Effects receptors and causes peripheral vasoconstriction this level
of epinephrine is probably never reached except when it is
When the sympathetic nervous system is activated the ad administered as a drug
renal medulla releases epinephrine 90 and norepi Denervated organs such as transplanted hearts are very
nephrine 10 which circulate in the blood see Chap responsive to circulating levels of epinephrine and norepi
ter 6 Changes in the circulating NE concentration are nephrine This increased sensitivity to neurotransmitters is
small relative to changes in NE resulting from the direct re referred to as denervation hypersensitivity Several factors
lease from nerve endings close to vascular smooth muscle contribute to denervation hypersensitivity including the
and cardiac cells Increased circulating epinephrine how absence of sympathetic nerve endings to take up circulating
ever contributes to skeletal muscle vasodilation during the norepinephrine and epinephrine actively leaving more
fight or flight response and exercise In these cases epi transmitter available for binding to receptors In addition
nephrine binds to 2 adrenergic receptors of skeletal mus denervation results in up regulation of neurotransmitter re
cle arteriolar smooth muscle cells and causes relaxation In ceptors in target cells During exercise circulating levels of
the heart circulating epinephrine binds to cardiac cell 1 norepinephrine and epinephrine increase Because of their
adrenergic receptors and reinforces the effect of NE re enhanced response to circulating catecholamines trans
leased from sympathetic nerve endings planted hearts can perform almost as well as normal hearts
A comparison of the responses to infusions of epineph
rine and norepinephrine illustrates not only the different
effects of the two hormones but also the different reflex re The Renin Angiotensin Aldosterone System
sponse each one elicits Fig 18 4 Epinephrine and norep Helps Regulate Blood Pressure and Volume
inephrine have similar direct effects on the heart but NE The control of total blood volume is extremely important
elicits a powerful baroreceptor reflex because it causes sys in regulating arterial pressure Because changes in total
blood volume lead to changes in central blood volume the
long term influence of blood volume on ventricular end di
Epinephrine Norepinephrine astolic volume and cardiac output is paramount Cardiac
output in turn strongly influences arterial pressure Hor
monal control of blood volume depends on hormones that
Cardiac output
regulate salt and water intake and output as well as red
blood cell formation
Reduced arterial pressure and blood volume cause the
5 5 release of renin from the kidneys Renin release is mediated
0 4 8 12 16 0 4 8 12 16 by the sympathetic nervous system and by the direct effect
of lowered arterial pressure on the kidneys Renin is a pro
Systemic vascular
15 19 teolytic enzyme that catalyzes the conversion of an
giotensinogen a plasma protein to angiotensin I
Fig 18 5 Angiotensin I is then converted to angiotensin
II by angiotensin converting enzyme ACE primarily in
10 14 the lungs Angiotensin II has the following actions
0 4 8 12 16 0 4 8 12 16 It is a powerful arteriolar vasoconstrictor and in some
circumstances it is present in plasma in concentrations
pressure mm Hg
150 150 sufficient to increase SVR
Arterial blood
It reduces sodium excretion by increasing sodium reab
100 Mean 100 sorption by proximal tubules of the kidney
Diastolic It causes the release of aldosterone from the adrenal cor
0 4 8 12 16 0 4 8 12 16 It causes the release of AVP from the posterior pituitary
Time min Time min gland
A comparison of the effects of intravenous Angiotensin II is a significant vasoconstrictor in some
FIGURE 18 4 circumstances Angiotensin II directly stimulates contrac
infusions of epinephrine and norepineph
rine See text for details Modified from Rowell LB Human tion of vascular smooth muscle and also augments NE re
Circulation Regulation During Physical Stress New York Ox lease from sympathetic nerves and sensitizes vascular
ford University Press 1986 smooth muscle to the constrictor effects of NE It plays an
CHAPTER 18 Control Mechanisms in Circulatory Function 297
Angiotensinogen Adrenal Aldosterone
cortex release
ACE Renal Decreased blood volume
Angiotensin I Angiotensin II proximal sodium and
tubule excretion arterial pressure
Peripheral Increased
arterioles SVR
FIGURE 18 5 Renin angiotensin aldosterone system This system plays an important role in the regu
lation of arterial blood pressure and blood volume ACE angiotensin converting enzyme
SVR systemic vascular resistance
important role in increasing SVR as well as blood volume cells and released into the bloodstream when the atria are
in individuals on a low salt diet If an ACE inhibitor is given stretched By increasing sodium excretion it decreases
to such individuals blood pressure falls Renin is released blood volume see Chapter 24 It also inhibits renin release
during blood loss even before blood pressure falls and the as well as aldosterone and AVP secretion Increased ANP
resulting rise in plasma angiotensin II increases the SVR along with decreased aldosterone and AVP may be par
One of the effects of aldosterone is to reduce renal ex tially responsible for the reduction in blood volume that
cretion of sodium the major cation of the extracellular occurs with prolonged bed rest When central blood vol
fluid Retention of sodium paves the way for increasing ume and atrial stretch are increased ANP secretion rises
blood volume Renin angiotensin aldosterone and the leading to higher sodium excretion and a reduction in
factors that control their release and formation are dis blood volume
cussed in Chapter 24 The RAAS is important in the normal
maintenance of blood volume and blood pressure It is crit
ical when salt and water intake is reduced Erythropoietin Increases the Production
Rarely renal artery stenosis causes hypertension that of Erythrocytes
can be attributed solely to elevated renin and angiotensin II The final step in blood volume regulation is production of
levels In addition the renin angiotensin system plays an erythrocytes Erythropoietin is a hormone released by the
important but not unique role in maintaining elevated kidneys that causes bone marrow to increase production of
pressure in more than 60 of patients with essential hy red blood cells raising the total mass of circulating red
pertension In patients with congestive heart failure renin cells The stimuli for erythropoietin release include hy
and angiotensin II are increased and contribute to elevated poxia and reduced hematocrit An increase in circulating
SVR as well as sodium retention AVP and aldosterone enhances salt and water retention and
results in an elevated plasma volume The increased plasma
Arginine Vasopressin Contributes volume with a constant volume of red blood cells results
to the Regulation of Blood Volume in a lower hematocrit The decrease in hematocrit stimu
lates erythropoietin release which stimulates red blood cell
Arginine vasopressin AVP is released by the posterior pi synthesis and therefore balances the increase in plasma
tuitary gland controlled by the hypothalamus Three pri volume with a larger red blood cell mass
mary classes of stimuli lead to AVP release increased
plasma osmolality decreased baroreceptor and cardiopul
monary receptor firing and various types of stress such as
physical injury or surgery In addition circulating an COMPARISON OF SHORT TERM AND
giotensin II stimulates AVP release Although AVP is a LONG TERM BLOOD PRESSURE CONTROL
vasoconstrictor it is not ordinarily present in plasma in Different mechanisms are responsible for the short term
high enough concentrations to exert an effect on blood and long term control of blood pressure Short term con
vessels However in special circumstances e g severe trol depends on activation of neural and hormonal re
hemorrhage it probably contributes to increased SVR sponses by the baroreceptor reflexes described earlier
AVP exerts its major effect on the cardiovascular system by Long term control depends on salt and water excretion
causing the retention of water by the kidneys see Chapter by the kidneys Excretion of salt and water by the kidneys
24 an important part of the neural and humoral mecha is regulated by some neural and hormonal mechanisms
nisms that regulate blood volume most of which have been mentioned earlier in this chapter
However it is also regulated by arterial pressure Increased
Atrial Natriuretic Peptide Helps Regulate arterial pressure results in increased excretion of salt and
water a phenomenon known as pressure diuresis Fig
Blood Volume
18 6 Because of pressure diuresis as long as mean arterial
Atrial natriuretic peptide ANP is a 28 amino acid pressure is elevated salt and water excretion will exceed the
polypeptide synthesized and stored in the atrial muscle normal rate this will tend to lower extracellular fluid vol
Arterial pressure Salt and An integrated view of the cardiovascular system requires an
increase water output understanding of the relationships among cardiac output
decrease venous return and central blood volume and how these re
lationships are influenced by interactions among various
Cardiac output
neural hormonal and other control mechanisms Consid
Plasma volume eration of the responses to standing erect provides an op
portunity to explore these elements in detail Figure 18 7
Central blood Blood volume compares venous pressures for the recumbent and standing
volume positions When a person is recumbent pressure in the
veins of the legs is only a few mm Hg above the pressure in
8 the right atrium The pressure distending the veins trans
mural pressure is equal to the pressure within the veins of
the legs because the pressure outside the veins is atmos
Output of salt and water
6 pheric pressure the zero reference pressure
times normal
When a person stands the column of blood above the
lower extremities raises venous pressure to about 50 mm
4 Hg at the femoral level and 90 mm Hg at the foot This is
50 100 150 200 250
Arterial pressure mm Hg
Regulation of arterial pressure by pressure
diuresis A higher output of salt and water in
response to increased arterial pressure reduces blood volume
Blood volume is reduced until pressure returns to its normal
level The curve on the left shows the relationship in a person
with normal blood pressure The curve on the right shows the
same relationship in an individual who is hypertensive Note
that the hypertensive individual has an elevated arterial pres
sure at a normal output of salt and water Modified from Guy
ton AC Hall JE Medical Physiology 10th Ed Philadelphia
WB Saunders 2000 p 203
ume and ultimately blood volume As discussed earlier in
this chapter and in Chapter 15 a decrease in blood volume
reduces stroke volume by lowering the end diastolic filling
of the ventricles Decreased stroke volume lowers cardiac
output and arterial pressure Pressure diuresis persists until
it lowers blood volume and cardiac output sufficiently to
return mean arterial pressure to a set level A decrease in
mean arterial pressure has the opposite effect on salt and
water excretion Reduced pressure diuresis increases blood
volume and cardiac output until mean arterial pressure is re
turned to a set level
Pressure diuresis is a slow but persistent mechanism for
regulating arterial pressure Because it persists in altering
salt and water excretion and blood volume as long as arte FIGURE 18 7
Venous pressures in the recumbent and
standing positions In this example standing
rial pressure is above or below a set level it will eventually places a hydrostatic pressure of approximately 80 mm Hg on the
return pressure to that level In hypertensive patients the feet Right atrial pressure is lowered because of the reduction in
curve shown in Figure 18 6 is shifted to the right so that central blood volume The negative pressures above the heart with
salt and water excretion are normal at a higher arterial pres standing do not actually occur because once intravascular pressure
sure If this were not the case pressure diuresis would inex drops below atmospheric pressure the veins collapse These are
orably bring arterial pressure back to normal the pressures that would exist if the veins remained open
CHAPTER 18 Control Mechanisms in Circulatory Function 299
the transmural distending pressure because the outside liter of blood It follows that an adequate cardiovascular re
pressure is still zero atmospheric Because the veins are sponse to the changes caused by upright posture or
highly compliant such a large increase in transmural pres thostasis is absolutely essential to our lives as bipeds see
sure is accompanied by an increase in venous volume Clinical Focus Box 18 1
The arteries of the legs undergo exactly the same in The immediate cardiovascular adjustments to upright
creases in transmural pressure However the increase in posture are the baroreceptor and cardiopulmonary recep
their volume is minimal because the compliance of the sys tor initiated reflexes followed by the muscle and respira
temic arterial system is only 1 20th that of the systemic ve tory pumps and later adjustments in blood volume
nous system Standing increases pressure in the arteries and
veins of the legs by exactly the same amount so the added
pressure has no influence on the difference in pressure driv Standing Elicits Baroreceptor
ing blood flow from the arterial to the venous side of the and Cardiopulmonary Reflexes
circulation It only influences the distension of the veins The decreased central blood volume caused by standing in
cludes reduced atrial ventricular and pulmonary vessel
Standing Requires a Complex volumes These volume reductions unload the cardiopul
Cardiovascular Response monary receptors and elicit a cardiopulmonary reflex Re
duced left ventricular end diastolic volume decreases stroke
When a person stands and the veins of the legs are dis volume and pulse pressure as well as cardiac output and
tended blood that would normally be returned toward the mean arterial pressure leading to decreased firing of aortic
right atrium remains in the legs filling the expanding veins arch and carotid baroreceptors The combined reduction in
For a few seconds after standing venous return to the heart firing of cardiopulmonary receptors and baroreceptors re
is lower than cardiac output and during this time there is sults in a reflex decrease in parasympathetic nerve activity
a net shift of blood from the central blood volume to the and an increase in sympathetic nerve activity to the heart
veins of the legs When a person stands up the heart rate generally in
When a 70 kg person stands central blood volume is creases by about 10 to 20 beats min The increased sympa
quickly reduced by approximately 550 mL If no compen thetic nerve activity to the ventricular myocardium shifts
satory mechanisms existed this would significantly reduce the ventricle to a new function curve and despite the low
cardiac end diastolic volume and cause a more than 60 ered ventricular filling stroke volume is decreased to only
decrease in stroke volume cardiac output and blood pres 50 to 60 of the recumbent value In the absence of the
sure the resulting fall in cerebral blood flow would proba compensatory increase in sympathetic nerve activity
bly cause a loss of consciousness If the individual contin stroke volume would fall much more These cardiac adjust
ues to stand quietly for 30 minutes 20 of plasma volume ments maintain cardiac output at 60 to 80 of the recum
is lost by net filtration through the capillary walls of the bent value An increase in sympathetic activity also causes
legs Therefore quiet standing for half an hour without arteriolar constriction and increased SVR The effect of
compensation is the hemodynamic equivalent of losing a these compensatory changes in heart rate ventricular con
Hypotension include vasodilation caused by alcohol vasodilating drugs
Baroreceptors volume receptors chemoreceptors and or fever cardiac disease e g cardiomyopathy valvular dis
pain receptors all help maintain adequate blood pressure ease or reduced blood volume secondary to hemorrhage
during various forms of hemodynamic stress such as dehydration or other causes of fluid loss In many patients
standing and exercise However in the presence of certain multiple causative factors are involved
cardiovascular abnormalities these mechanisms may fail The treatment of symptomatic hypotension is to elimi
to regulate blood pressure appropriately when this oc nate the underlying cause whenever possible which in
curs a person may experience transient or sustained hy some cases produces satisfactory results When this ap
potension As a practical definition hypotension exists proach is not possible other adjunctive measures may be
when symptoms are caused by low blood pressure and in necessary especially when the symptoms are disabling
extreme cases hypotension may cause weakness light Common treatment modalities include avoidance of fac
headedness or even fainting tors that can precipitate hypotension e g sudden
Hypotension may be due to neurogenic or nonneuro changes in posture hot environments alcohol certain
genic factors Neurogenic causes include autonomic dys drugs large meals volume expansion using salt supple
function or failure which can occur in association with other ments and or medications with salt retaining volume ex
central nervous system abnormalities such as Parkinson s panding properties and mechanical measures including
disease or may be secondary to systemic diseases that can tight fitting elastic compression stockings or pantyhose to
damage the autonomic nerves such as diabetes or amyloi prevent the blood from pooling in the veins of the legs
dosis vasovagal hyperactivity hypersensitivity of the upon standing Unfortunately even when these measures
carotid sinus and drugs with sympathetic stimulating or are employed some patients continue to have severe de
blocking properties Nonneurogenic causes of hypotension bilitating effects from hypotension
tractility and SVR is maintenance of mean arterial pressure to standing A more powerful activation of the barorecep
In fact mean arterial pressure may be increased slightly tor reflex as occurs during severe hemorrhage is required to
above the recumbent value cause significant venoconstriction However two other
How is increased sympathetic nerve activity maintained if mechanisms return blood from the legs to the central blood
the mean arterial pressure reaches a value near or above that volume The more important mechanism is the muscle
of the recumbent value In other words why doesn t the pump Fig 18 8 If the leg muscles periodically contract
sympathetic nerve activity return to recumbent levels if the while an individual is standing venous return is increased
mean arterial pressure returns to the recumbent value There Muscles swell as they shorten and this compresses adjacent
are two reasons First although the mean arterial pressure re veins Because of the venous valves in the limbs the blood
turns to the same level or even higher pulse pressure re in the compressed veins can flow only toward the heart
mains reduced because the stroke volume is decreased to 50 The combination of contracting muscle and venous valves
to 60 of the recumbent value As indicated earlier the fir provides an effective pump that transiently increases ve
ing rate of the baroreceptors depends on both mean arterial nous return relative to cardiac output This mechanism
and pulse pressures Reduced pulse pressure means the shifts blood volume from the legs to the central blood vol
baroreceptor firing rate is reduced even if the mean arterial ume and end diastolic volume is increased Even mild ex
pressure is slightly higher Second although mean arterial ercise such as walking returns the central blood volume
pressure is returned to the recumbent value central blood and stroke volume to recumbent values Fig 18 9
volume remains low Consequently the cardiopulmonary re The respiratory pump is the other mechanism that acts
ceptors continue to discharge at a lower rate leading to in to enhance venous return and restore central blood volume
creased sympathetic activity Some investigators believe it is Fig 18 10 Quiet standing for 5 to 10 minutes invariably
the decreased stretch of the cardiopulmonary receptors that leads to sighing This exaggerated respiratory movement
provides the primary steady state afferent information for the lowers intrathoracic pressure more than usually occurs with
reflex cardiovascular response to standing inspiration The fall in intrathoracic pressure raises the
The heart and brain do not participate in the arteriolar transmural pressure of the intrathoracic vessels causing
constriction caused by increased sympathetic nerve activity these vessels to expand Contraction of the diaphragm si
during standing therefore the blood flow and supply of oxy multaneously raises intraabdominal pressure which com
gen and nutrients to these two vital organs are maintained presses the abdominal veins Because the venous valves pre
vent the backflow of blood into the legs the raised
Muscle and Respiratory Pumps Help intraabdominal pressure forces blood toward the intratho
racic vessels which are expanding because of the lowered
Maintain Central Blood Volume
intrathoracic pressure The seesaw action of the respiratory
Although standing would appear to be a perfect situation pump tends to displace extrathoracic blood volume toward
for increased venoconstriction which could return some of the chest and raise right atrial pressure and stroke volume
the blood from the legs to the central blood volume reflex Figure 18 11 provides an overview of the main cardiovascu
venoconstriction is a relatively minor part of the response lar events associated with a short period of standing
During Just after
contraction contraction
Just before
Artery Vein
Arterial pressure Venous pressure
90 93 mm Hg 90 10 mm Hg 90 93 mm Hg 20 10 mm Hg
FIGURE 18 8 Muscle pump This mechanism increases ve static column of blood lowering venous and capillary hydro
nous return and decreases venous volume The static pressure
valves which are closed after contraction break up the hydro
CHAPTER 18 Control Mechanisms in Circulatory Function 301
Prone Erect Walking
Arterial 110
blood pressure
Right atrial
mean pressure 0 2 5 1
Cardiac output
L min 5 SVR 16 21 16
Stroke volume FIGURE 18 10 Respiratory pump Inspiration leads to an
mL increase in venous return and stroke volume
50 Small type represents a secondary change that returns variables
toward the original values
blood volume 1 0
0 8 Capillary Filtration During Standing Further
Reduces Central Blood Volume
During quiet minimum muscular movement standing for
Heart rate 10 to 15 minutes the effects of the baroreceptor reflex on
beats min 70 the heart and arterioles are insufficient to prevent a contin
60 ued decline in arterial pressure The decline in arterial pres
sure is caused by a steady loss of plasma volume as fluid fil
ters out of capillaries of the legs The hydrostatic column of
Forearm Total
blood flow 2 0
mL 100 Muscle
mL 1 min 1
blood flow 1 0
0 2 4 6 8 10
Effect of the muscle pump on central blood
volume and systemic hemodynamics The
center section shows the effects of a shift from the prone to the
upright position with quiet standing The right panel shows the
effect of activating the muscle pump by contracting leg muscles
Note that the muscle pump restores central blood volume and
cardiac output to the levels in the prone position The fall in heart
rate and rise in peripheral blood flow forearm splanchnic and
renal associated with activation of the muscle pump reflect the
reduction in baroreceptor reflex activity associated with increased
cardiac output RVEDP right ventricular end diastolic pressure
SVR systemic vascular resistance Modified from Rowell LB Hu
man Circulation Regulation During Physical Stress New York
Oxford University Press 1986
FIGURE 18 11
Cardiovascular events associated with
standing Small type represents compensatory
changes that return variables toward the original values 1 and
1 refer to adrenergic receptor types
blood above the capillaries of the legs and feet raises capil translocation of plasma volume into the interstitial space
lary hydrostatic pressure and filtration During a period of see Chapter 16 These factors together with neural and
30 minutes a 10 loss of blood volume into the interstitial myogenic responses and the muscle and respiratory pumps
space can occur This loss coupled with the 550 mL dis play a significant role during the seconds and minutes fol
placed by redistribution from the central blood volume into lowing standing Fig 18 12 The combination of all of
the legs causes central blood volume to fall to a level so low these factors minimizes net capillary filtration making it
that reflex sympathetic nerve activity cannot maintain car possible to remain standing for long periods
diac output and mean arterial pressure Diminished cerebral
blood flow and a loss of consciousness fainting result
Arteriolar constriction due to the increased reflex sym Long Term Responses Defend Venous
pathetic nerve activity tends to reduce capillary hydrostatic Return During Prolonged Upright Posture
pressure However this alone does not bring capillary hy In addition to the relatively short term cardiovascular re
drostatic pressure back to normal because it does not affect sponses there are equally important long term adjustments
the hydrostatic pressure exerted on the capillaries from the to orthostasis These are observed in patients confined to
venous side The muscle pump is the most important factor bed or astronauts not subject to the force of gravity In
counteracting increased capillary hydrostatic pressure The people who are bedridden intermittent upright posture
alternate compression and filling of the veins as the muscle does not shift the distribution of blood volume from the
pump works means the venous valves are closed most of the thorax to the legs During the course of a day average cen
time When the valves are closed the hydrostatic column tral blood volume and pressure is greater than in a person
of blood in the leg veins at any point is only as high as the who is periodically standing up in the presence of gravity
distance to the next valve The average increase in central blood volume caused by ex
The myogenic response of arterioles to increased trans
mural pressure also acts to oppose filtration As discussed
earlier raising the transmural pressure stretches vascular
smooth muscle and stimulates it to contract This is espe Blood
cially true for the myocytes of precapillary arterioles The volume
Atrial Arterial
elevated transmural pressure associated with standing causes volume pressure
a myogenic response and decreases the number of open cap
illaries With fewer open capillaries the filtration rate for a AVP ANP Medullary cardiovascular
center increased
given capillary hydrostatic pressure imbalance is less sympathetic nerve firing
In addition to the factors cited above other safety fac
tors against edema are important for preventing excessive
receptors receptors
Sodium load
distal tubules
Stretch of
Renin release afferent
Angiotensin I Peritubular
Angiotensin II hydrostatic
Aldosterone Plasma
Sodium excretion
Water excretion Extracellular
fluid volume
Intake of sodium
FIGURE 18 13 Regulation of blood volume Blood loss in
fluences sodium and water excretion by the
kidney via several pathways All these pathways combined with
an increased intake of salt and water restore the extracellular fluid
FIGURE 18 12 Effects of prolonged standing With pro volume and eventually blood volume These responses occur
longed standing capillary filtration reduces ve later than those shown in Figures 18 10 18 11 and 18 12 The
nous return Without the compensatory events that result in the pathways responsible for stimulating an increased intake of salt
changes shown in small type prolonged standing would in and water are not shown AVP arginine vasopressin ANP atrial
evitably lead to fainting natriuretic peptide GFR glomerular filtration rate
CHAPTER 18 Control Mechanisms in Circulatory Function 303
tended bed rest results in reduced activity of all of the path Aldosterone acts on the distal nephron to cause in
ways that increase blood volume in response to standing creased reabsorption of sodium and thereby decrease its
The reduction in total blood volume begins during the first excretion Aldosterone released from the adrenal cortex
day and is quantitatively significant after a few days At this is increased by among other things angiotensin II Wa
point standing becomes difficult because blood volume is ter intake is determined by thirst and the availability of
not adequate to sustain a normal blood pressure Looking at water
it another way maintaining an erect posture in the earth s The excretion of water is strongly influenced by AVP
gravitational field results in increased blood volume This Increased plasma osmolality sensed by the hypothalamus
increase proportioned between the extrathoracic and in results in both thirst and increased AVP release Thirst and
trathoracic vessels augments stroke volume during stand AVP release are also increased by decreased stretch of
ing If blood volume is not maintained by intermittent erect baroreceptors and cardiopulmonary receptors
posture standing becomes extremely difficult or impossible Consider how these physiological variables are al
because of orthostatic hypotension diminished blood tered by an upright posture to produce an increase in the
pressure associated with standing extracellular fluid volume Renal arteriolar vasoconstric
The long term regulation of blood volume is driven by tion associated with increased sympathetic nerve activ
changes in plasma volume accomplished by sympathetic ity produced by standing reduces the glomerular filtra
nervous system effects on the kidneys hormonal changes tion rate This results in a decrease in filtered sodium and
including RAAS AVP and ANP and alterations in pressure tends to decrease sodium excretion The increased sym
diuresis Figure 18 13 depicts several components of plasma pathetic nerve activity to the kidney also triggers the re
volume regulation by showing their response to a moderate lease of renin which increases circulating angiotensin II
approximately 10 blood loss which is easily compen and in turn aldosterone release The decrease in central
sated for in healthy individuals blood volume associated with standing reduces car
Plasma is a part of the extracellular compartment and is diopulmonary stretch receptor activity causing an in
subject to the factors that regulate the size of that space The creased release of AVP from the posterior pituitary
osmotically important electrolytes of the extracellular fluid Therefore both sodium and water are retained and thirst
are the sodium ion and its main partner the chloride ion The is increased Regulation of the precise quantities of wa
control of extracellular fluid volume is determined by the bal ter and sodium that are excreted maintains the correct
ance between the intake and excretion of sodium and water osmolality of the plasma
This topic is discussed in depth in Chapter 24 Sodium excre The distribution of extracellular fluid between plasma
tion is much more closely regulated than sodium intake Ex and interstitial compartments is determined by the balance
cretion of sodium is determined by the glomerular filtration of hydrostatic and colloid osmotic forces across the capil
rate the plasma concentrations of aldosterone and ANP and lary wall Retention of sodium and water tends to dilute
a variety of other factors including angiotensin II plasma proteins decreasing plasma colloid osmotic pres
Glomerular filtration rate is determined by glomerular sure and favoring the filtration of fluid from the plasma into
capillary pressure which is dependent on precapillary af the interstitial fluid However as increased synthesis of
ferent arteriolar and postcapillary efferent arteriolar re plasma proteins by the liver occurs a portion of the re
sistance and arterial pressure Decreased mean arterial pres tained sodium and water contributes to an increase in
sure and or afferent arteriolar constriction tends to result in plasma volume
lowered glomerular capillary pressure less filtration of Finally the increase in plasma volume in the absence of
fluid and lower sodium excretion Changes in glomerular any change in total red cell volume decreases hematocrit
capillary pressure are primarily the result of changes in which stimulates erythropoietin release and erythropoiesis
sympathetic nerve activity and plasma angiotensin II and This helps total red blood cell volume keep pace with
ANP concentrations plasma volume
DIRECTIONS Each of the numbered B High sensitivity of arterioles to B Lower the heart rate below its
items or incomplete statements in this norepinephrine intrinsic rate
section is followed by answers or by C High sensitivity of arterioles to C Raise and lower the heart
completions of the statement Select the nitric oxide rate above and below its intrinsic
ONE lettered answer or completion that is D Low parasympathetic nerve rate
BEST in each case activity D Neither raise nor lower the heart
E Arterioles insensitive to rate from its intrinsic rate
1 A person has cold painful fingertips epinephrine 3 The cold pressor response is initiated
because of excessively constricted 2 In the presence of a drug that blocks by stimulation of
blood vessels in the skin Which of all effects of norepinephrine and A Baroreceptors
the following alterations in autonomic epinephrine on the heart the B Cardiopulmonary receptors
function is most likely to be involved autonomic nervous system can C Hypothalamic receptors
A Low concentration of circulating A Raise the heart rate above its D Pain receptors
epinephrine intrinsic rate E Chemoreceptors
4 Which of the following occurs when heart accompanied by a withdrawal of D Lying down
acetylcholine binds to muscarinic sympathetic tone to most of the blood E Living in a space station
receptors vessels of the body is characteristic of
A Heart rate slows A The fight or flight response SUGGESTED READING
B Cardiac conduction velocity rises B Vasovagal syncope Champleau MW Arterial baroreflexes In
C Norepinephrine release from C Exercise Izzo JL Black HR eds Hypertension
sympathetic nerve terminals is D The diving response Primer Baltimore Lippincott Williams
enhanced E The cold pressor response Wilkins 1999
D Nitric oxide release from 8 A patient suffers a severe hemorrhage Dampney RA Functional organization of
endothelial cells is inhibited resulting in a lowered mean arterial central pathways regulating the cardio
E Blood vessels of the external pressure Which of the following vascular system Physiol Rev
genitalia constrict would be elevated above normal levels 1994 74 323 364
5 Carotid baroreceptors A Splanchnic blood flow Hainsworth R Mark AL eds Cardiovascu
A Are important in the rapid short B Cardiopulmonary receptor activity lar Reflex Control in Health and Dis
term regulation of arterial blood C Right ventricular end diastolic ease London WB Saunders 1993
pressure volume Katz AM Physiology of the Heart 3rd
B Do not fire until a pressure of D Heart rate Ed New York Lippincott Williams
approximately 100 mm Hg is reached E Carotid baroreceptor activity Wilkins 2001
C Adapt over 1 to 2 weeks to the 9 A person stands up Compared with Mohanty PK Cardiopulmonary barore
prevailing mean arterial pressure the recumbent position 1 minute after flexes In Izzo JL Black HR eds Hy
D Stretch reflexively decreases standing the pertension Primer Baltimore Lippin
cerebral blood flow A Skin blood flow increases cott Williams Wilkins 1999
E Reflexively decrease coronary B Volume of blood in leg veins Reis DJ Functional neuroanatomy of cen
blood flow when blood pressure falls increases tral vasomotor control centers In Izzo
6 Which of the following is true with C Cardiac preload increases JL Black HR eds Hypertension
respect to peripheral chemoreceptors D Cardiac contractility decreases Primer Baltimore Lippincott Williams
A Activation is important in E Brain blood flow decreases Wilkins 1999
inhibiting the diving response 10 Pressure diuresis lowers arterial Rowell LB Human Cardiovascular Con
B Activity is increased by increased pressure because it trol New York Oxford University
pH A Lowers renal release of renin Press 1993
C They are located in the medulla B Lowers systemic vascular resistance Waldrop TG Eldridge FL Iwamoto GA
oblongata but not the hypothalamus C Lowers blood volume Mitchell JH Central neural control of
D Activation is important in the D Causes renal vasodilation respiration and
cardiovascular response to E Increases baroreceptor firing circulation during exercise In Rowell LB
hemorrhagic hypotension 11 Central blood volume is decreased by Shepherd JT eds Handbook of Physi
E Activity is increased by lowering A The muscle pump ology Section 12 Exercise Regulation
of the oxygen content but not the B The respiratory pump and integration of multiple systems
PO2 of arterial blood C Increased excretion of salt and New York Oxford University Press
7 Parasympathetic stimulation of the water 1996
CASE STUDY FOR CHAPTER 11 Answers to Case Study Questions for Chapter 11
1 The disease chronic granulomatous disease of child
Chronic Granulomatous Disease of Childhood hood results from a congenital lack of the superoxide
An 18 month old boy with a high fever and cough and forming enzyme NADPH oxidase in this patient s neu
with a history of frequent infections was brought to the trophils The lack of this enzyme results in deficient
emergency department by his father A blood examina hydrogen peroxide generation by these cells when they
tion shows elevated numbers of neutrophils but no ingest or phagocytose bacteria resulting in a compro
other defects A blood culture for bacteria is positive mised capacity to combat recurrent life threatening bac
The physician sent a sample of the boy s blood to a labo terial infections
ratory to test the ability of the patient s neutrophils to 2 Normal neutrophil stem cells grown in culture may be in
produce hydrogen peroxide The ability of this patient s fused to supplement the patient s own defective neu
neutrophils to generate hydrogen peroxide is found to trophils In addition researchers are now trying to geneti
be completely absent cally reverse the defect in cultures of a patient s stem
cells for subsequent therapeutic infusion
1 What cellular defect may have led to the complete absence Reference
of hydrogen peroxide generation in this patient s neu Baehner RL Chronic granulomatous disease of childhood
trophils Clinical pathological biochemical molecular and genetic
2 How might this disease be treated using hematotherapy aspects of the disease Pediatr Pathol 1990 10 143 153

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