for the renin-angiotensin-aldosterone system.
decreases aldosterone release by the adrenal
cortex; increases glomerular filtration rate;
produces natriuresis and diuresis (potassium
sparing); and decreases renin release, thereby
reduce blood volume, which leads to a fall in
central venous pressure, cardiac output, and
arterial blood pressure. Chronic elevations of
ANP appear to decrease arterial blood pres-
sure primarily by decreasing systemic vascu-
lar resistance.
The mechanism of systemic vasodilation
may involve ANP receptor-mediated eleva-
tions in vascular smooth muscle cGMP (ANP
activates particulate guanylyl cyclase). ANP
attenuates sympathetic vascular tone.
This latter mechanism may involve ANP acting
upon sites within the central nervous system
as well as through inhibition of norepineph-
rine release by sympathetic nerve terminals.
A new class of drugs that are neutral
endopeptidase (NEP) inhibitors is useful
in treating acute heart failure. By inhibiting
NEP, the enzyme responsible for the degra-
dation of ANP, these drugs elevate plasma
levels of ANP NEP inhibition is particularly
effective in some forms of heart failure when
combined with an ACE inhibitor. The reason
for this is that NEP inhibition, by elevating
ANP, reinforces the effects of ACE inhibition.
natriuretic peptide
32-amino acid peptide hormone related to
ANP, is synthesized and released by the ventri-
cles in response to pressure and volume over-
load, particularly during heart failure. BNP
appears to have actions that are similar to those
of ANP Circulating BNP is now used clinically
as a sensitive biomarker for heart failure.
Vasopressin (Antidiuretic
Vasopressin (arginine vasopressin, AVP; anti-
diuretic hormone, ADH) is a nonapeptide
hormone released from the posterior pitui-
tary (Fig. 6.13). AVP has two principal sites
of action: the kidneys and blood vessels. The
most important physiologic action of AVP is
that it increases water reabsorption by the
kidneys by increasing water permeability in
the collecting duct, thereby permitting the
formation of concentrated urine. This anti-
diuretic property of AVP, which acts through
renal V2 receptors, increases blood volume
and arterial blood pressure. This hormone
also constricts arterial blood vessels through
V1 vascular receptors; however, the normal
Angiotensin II
Decreased atrial receptor firing
Sympathetic stimulation
Arterial Pressure
Renal Fluid
Blood Volume
■ FIGURE 6.13 Cardiovascular and renal effects of arginine vasopressin (AVP). AVP release from the
posterior pituitary is stim ulated by angiotensin II, hyperosmolarity, decreased atrial receptor firing (usually
in response to hypovolemia), and sym pathetic activation. The primary action of AVP is on the kidney to
increase water reabsorption (antidiuretic effect), which increases blood volume. AVP also has direct vaso-
constrictor actions at high concentrations. Increased arterial pressure is the overall effect of increased AVP.
previous page 153 Cardiovascular Physiology Concepts  2nd Edition read online next page 155 Cardiovascular Physiology Concepts  2nd Edition read online Home Toggle text on/off