146
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
because reflex systemic vasodilation can
occur only if arterial pressure is elevated
and baroreceptor firing increases.
8.
The correct answer is “a” because
increased renin leads to increased angio-
tensin II and aldosterone (therefore,
choice “d” is incorrect), both of which
act on the kidney to increase sodium
reabsorption and blood volume (there-
fore, choice “c” is incorrect). Choice “b”
is incorrect because although circulating
atrial natriuretic peptide is increased,
this hormone counteracts the pressure-
elevating mechanisms of angiotensin II.
9.
The correct answer is “a” because atrial
natriuretic peptide produces natriuresis
and diuresis, both of which are ben-
eficial to the acutely decompensated
heart failure patient who has excessive
accumulation of fluid that can cause
pulmonary and systemic edema. Choices
“b,” “c,” and “d” are incorrect because
atrial natriuretic peptide dilates vessels,
reduces preload and cardiac output, and
decreases aldosterone release.
10. The correct answer is “b” because
vasopressin constricts blood vessels
directly through
W1
receptors, and not
through augmentation of sympathetic
activity which will actually decline as
pressure is elevated during vasopressin
administration (therefore, choice “a”
is incorrect). Choice “c” is incorrect
because vasopressin has an antidiuretic
effect. Choice “d” is incorrect because
circulating renin would decline as
pressure is elevated during vasopressin
administration.
ANSWERS TO PROBLEMS AND CASES
PROBLEM 6-1
The common carotid arteries are below the
carotid sinus haroreceptors. Therefore, occlu-
sion of both carotid arteries reduces pressure
within the carotid sinuses. This decreases
their firing,
leading to
increased sympa-
thetic and decreased vagal outflow from the
medulla. This results in systemic vasocon-
striction, cardiac stimulation, and a rise in
arterial pressure.
Bilateral vagotomy enhances the response
described above because as arterial pressure
rises during carotid occlusion, the aortic
arch haroreceptors, which are innervated by
the vagus nerve, increase their firing. This
partially counteracts the effects of decreased
carotid
sinus
firing.
Bilateral
vagotomy
removes this influence of the aortic arch
haroreceptors.
Blockade of P-adrenoceptors would prevent
the sympathetic-mediated increases in heart
rate and inotropy (although some withdrawal
of vagal tone may still result in a small increase
in heart rate). The pressor response would still
occur because of systemic vasoconstriction
((Xj-adrenoceptor
mediated);
however,
the
pressor response would be blunted significantly
because cardiac stimulation would be blocked.
PROBLEM 6-2
P^adrenoceptor
activation
is
primarily
responsible for the tachycardia and increased
cardiac
output produced by epinephrine.
Blocking
P-adrenoceptors
would
signifi-
cantly blunt the cardiac responses. Epineph-
rine at low plasma concentrations also binds
to vascular P2-adrenoceptors to cause vasodi-
lation; therefore, arterial pressure would fall
during infusion of a low dose of epinephrine
in the presence of P—adrenoceptor blockade
because the large decrease in systemic vas-
cular resistance would not be offset by an
increase in cardiac output.
PROBLEM 6-3
Bilateral cervical vagotomy would prevent
vagal slowing of the heart and denervate the
aortic arch haroreceptors. Heart rate (and
inotropy) would increase owing to norepi-
nephrine binding to P1
-adrenoceptors on the
heart that is now unopposed by the vagus.
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