CHAPTER 6 • NEUROHUMORAL CONTROL OF THE HEART AND CIRCULATION
141
physiologic concentrations of AVP are below
its vasoactive range. Studies have shown, nev-
ertheless, that in severe hypovolemic shock,
when AVP release is very high, AVP contrib-
utes to the compensatory increase in systemic
vascular
resistance.
This
vasoconstrictor
property of AVP is sometimes utilized in the
treatment of circulatory shock; AVP is admin-
istered to increase systemic vascular resist-
ance and therefore arterial pressure.
Several mechanisms regulate the release of
AVP. Specialized stretch receptors within the
atrial walls and large veins (cardiopulmonary
baroreceptors) entering the atria decrease their
firing rate when atrial pressure falls (as occurs
with hypovolemia). Afferents from these recep-
tors synapse within the hypothalamus, which
is the site of AVP synthesis. AVP is transported
from the hypothalamus via axons to the pos-
terior pituitary, from where it is secreted into
the circulation. Atrial receptor firing normally
inhibits the release of AVP With hypovolemia
and decreased central venous pressure, the
decreased firing of atrial stretch receptors
leads to an increase in AVP release. AVP release
is also stimulated by enhanced sympathetic
activity
accompanying
decreased
arterial
baroreceptor activity during hypotension. An
important mechanism regulating AVP release
involves hypothalamic osmoreceptors, which
sense extracellular osmolarity. When osmolar-
ity rises, as occurs during dehydration, AVP
release is stimulated, which increases water
retention by the kidneys. Finally, angiotensin
II receptors (AT:) located within the hypo-
thalamus regulate AVP release; an increase in
angiotensin II stimulates AVP release.
Heart failure causes a paradoxical increase
in AVP. The increased blood volume and atrial
pressure associated with heart failure suggest
that AVP secretion should be inhibited, but it
is not. It may be that sympathetic and renin-
angiotensin system activation in heart failure
override the volume and low-pressure cardio-
vascular receptors (as well as the osmoregula-
tion of AVP) and cause the increase in AVP
secretion. This increase in AVP during heart
failure may contribute to the increased sys-
temic vascular resistance and to renal reten-
tion of fluid.
In summary, the importance of AVP in
cardiovascular regulation is primarily through
its effects on volume regulation, which in
turn affects ventricular preload and cardiac
output through the Frank-Starling relationship.
Increased AVP, by increasing blood volume,
increases cardiac output and arterial pressure.
The vasoconstrictor effects of AVP are probably
important only when AVP levels are very high,
as occurs during severe hypovolemia.
INTEGRATION OF
NEUROHUMORAL MECHANISMS
Autonomic and humoral influences are neces-
sary to maintain a normal arterial blood pres-
sure under the different conditions in which
the human body functions.
Neurohumoral
mechanisms enable the body to adjust to
changes in body posture, physical activity, or
environmental conditions. The neurohumoral
mechanisms act through changes in systemic
vascular resistance, venous compliance, blood
volume, and cardiac function, and through
these actions, they can effectively regulate arte-
rial blood pressure (Table 6-2). Although each
mechanism has independent cardiovascular
actions, it is important to understand that each
mechanism also has complex interactions with
other control mechanisms that serve to rein-
force or inhibit the actions of the other control
mechanisms. For example, activation of sym-
pathetic nerves either directly or indirectly
increases circulating angiotensin II, aldoster-
one, adrenal catecholamines, and arginine vas-
opressin, which act together to increase blood
volume, cardiac output, and arterial pressure.
These humoral changes are accompanied by
an increase in ANP, which acts as a counter-
regulatory system to limit the effects of the
other neurohumoral mechanisms.
Finally, it is important to note that some
neurohumoral effects are rapid (e.g., auto-
nomic nerves and catecholamine effects on
cardiac output and arterial pressure), whereas
others may take several hours or days because
changes in blood volume must occur before
alterations in cardiac output and arterial pres-
sure can be fully expressed.
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