CHAPTER 33Cardiovascular Regulatory Mechanisms 567CIRCULATING VASOCONSTRICTORS
Vasopressin is a potent vasoconstrictor, but when it is injected
in normal individuals, there is a compensating decrease in car-
diac output, so that there is little change in blood pressure. Its
role in blood pressure regulation is discussed in Chapter 18.
Norepinephrine has a generalized vasoconstrictor action,
whereas epinephrine dilates the vessels in skeletal muscle and
the liver. The relative unimportance of circulating norepineph-
rine, as opposed to norepinephrine released from vasomotor
nerves, is pointed out in Chapter 22, where the cardiovascular
actions of catecholamines are discussed in detail.
Angiotensin II has a generalized vasoconstrictor action. It is
formed by the action of angiotensin converting enzyme (ACE)
on angiotensin I, which itself is liberated by the action of renin
from the kidney on circulating angiotensinogen (see Chapter
39). Renin secretion, in turn, is increased when the blood pres-
sure falls or extracellular fluid (ECF) volume is reduced, and
angiotensin II therefore helps to maintain blood pressure.
Angiotensin II also increases water intake and stimulates
aldosterone secretion, and increased formation of angiotensin
II is part of a homeostatic mechanism that operates to main-
tain ECF volume (see Chapter 22). In addition, there are ren-
nin–angiotensin systems in many different organs, and there
may be one in the walls of blood vessels. Angiotensin II pro-
duced in blood vessel walls could be important in some forms
of clinical hypertension. The role of angiotensin II in cardio-
vascular regulation is also amply demonstrated in the wide-
spread use of so-called ACE inhibitors as antihypertensive
medications.
Urotensin-II, a polypeptide first isolated from the spinal
cord of fish, is present in human cardiac and vascular tissue. It
is one of the most potent mammalian vasoconstrictors
known, but its pathophysiogic and physiologic roles are cur-
rently the subject of intense interest.
CHAPTER SUMMARY
■ RVLM neurons project to the thoracolumbar IML and release
glutamate on preganglionic sympathetic neurons that innervate
the heart and vasculature.
■ The NTS is the major excitatory input to cardiac vagal motor
neurons in the nucleus ambiguus.
■ Carotid sinus and aortic depressor baroreceptors are innervated
by branches of the 9th and 10th cranial nerves, respectively
(glossopharyngeal and aortic depressor nerves). These receptors
are most sensitive to changes in pulse pressure but also respond
to changes in mean arterial pressure.
■ Baroreceptor nerves terminate in the NTS and release glutamate.
NTS neurons project to the CVLM and nucleus ambiguus and
release glutamate. CVLM neurons project to RVLM and release
GABA. This leads to a reduction in sympathetic activity and an
increase in vagal activity (ie, the baroreceptor reflex).
■ Activation of peripheral chemoreceptors in the carotid and aor-
tic bodies by a reduction in PaO 2 or an increase in PaCO 2 leads
to an increase in vasoconstriction. Heart rate changes are vari-able and depend on a number of factors including changes in
respiration.
■ In addition to various neural inputs, RVLM neurons are directly
activated by hypoxia and hypercapnia.
■ Most vascular beds have an intrinsic capacity to respond to
changes in blood pressure within a certain range by altering
vascular resistance to maintain stable blood flow. This property
is known as autoregulation.
■ Local factors such as oxygen tension, pH, temperature, and
metabolic products contribute to vascular regulation; many
produce vasodilation to restore blood flow.
■ The endothelium is an important source of vasoactive media-
tors that act to either contract or relax vascular smooth muscle.
■ Three gaseous mediators—NO, CO, and H 2 S—are important
regulators of vasodilation.
■ Endothelins and angiotensin II induce vasoconstriction and may
be involved in the pathogenesis of some forms of hypertension.MULTIPLE-CHOICE QUESTIONS
For all questions, select the single best answer unless otherwise directed.- When a pheochromocytoma (tumor of the adrenal medulla)
suddenly discharges a large amount of epinephrine into the cir-
culation, the patient’s heart rate would be expected to
A) increase, because the increase in blood pressure stimulates
the carotid and aortic baroreceptors.
B) increase, because epinephrine has a direct chronotropic
effect on the heart.
C) increase, because of increased tonic parasympathetic
discharge to the heart.
D) decrease, because the increase in blood pressure stimulates
the carotid and aortic chemoreceptors.
E) decrease, because of increased tonic parasympathetic
discharge to the heart. - Activation of the baroreceptor reflex
A) is primarily involved in short-term regulation of systemic
blood pressure.
B) leads to an increase in heart rate because of inhibition of the
vagal cardiac motor neurons.
C) inhibits neurons in the CVLM.
D) excites neurons in the RVLM.
E) all of the above - Sympathetic nerve activity would be expected to increase
A) if glutamate receptors were blocked in the NTS.
B) if GABA receptors were blocked in the RVLM.
C) if there was a compression of the RVLM.
D) during hypoxia.
E) for all of the above. - Why is the dilator response to injected acetylcholine changed to
a constrictor response when the endothelium is damaged?
A) More Na+ is generated.
B) More bradykinin is generated.
C) The damage lowers the pH of the remaining layers of the
artery.
D) The damage augments the production of endothelin by the
endothelium.
E) The damage interferes with the production of NO by the
endothelium.