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564 PA R T I V / Pathophysiology and Management of Heart Disease
Sympathetic ■ Figure 24-9 The renin–
efferent activity angiotensin–aldosterone system is
activated in patients with heart fail-
ure. Multiple stimuli may con-
Diuretic
therapy tribute to renal release of renin into
the systemic circulation, including
increased sympathetic efferent ac-
Distal tubular tivity, decreased tubular sodium de-
Angiotensinogen sodium load livery, reduced renal perfusion, and
(liver) diuretic therapy. Natriuretic pep-
Renin Renal perfusion tides (ANP, BNP), and vasopressin
release pressure (ADH) (striped arrows) may inhibits s
release of renin. Angiotensin I is
Angiotensin I
2+
Angiotensin- Other (K -Ca ) converted to angiotensin II, which
+
converting prostaglandins is a potent vasoconstrictor; it pro-
enzyme motes sodium reabsorption by in-
creasing aldosterone secretion, and
Angiotensin II
ANP, BNP
by a direct effect on the tubules,
stimulates water intake by acting
Thirst Sodium on the thirst center. (Adapted from
retention Vasopressin Paganelli, W. C., Craeger, M. A., &
(direct Dzau, V. J. [1986]. Cardiac regula-
tubular Aldosterone
effect) secretion tion of renal function. In T. O.
Cheung [Ed.], International text-
book of cardiology. New York:
Vasoconstriction
Bergamman Press.)
cell growth (hypertrophy), and apoptosis (programmed cell relaxes smooth muscle; this vasodilatation lowers peripheral resist-
death). The AT2 receptor, a “fetal phenotype,” promotes counter- ance and dilates renal blood vessels. Prostaglandin synthesis is
regulatory effects, including vasodilatation and decrease in growth stimulated by NE, AT, and ADH. The vasodilators are prostacy-
and proliferation of cells. The AT1 receptor is downregulated in clin (PGI 2 ) and prostaglandin E 2 . Because they are short-lived,
patients with HF. 24 they act locally to exert their effects, either released from one cell
ADH is a pituitary hormone that plays a central role in regu- to work on another (paracrine effect) or binding to the same cell
lation of plasma osmolality and free water clearance. It is released that released the prostaglandin (autocrine effect). In patients with
into the circulation in response to hyperosmolarity and AT. It HF, these counter-regulatory effects are often overwhelmed by the
causes vasoconstriction via vasopressin 1 receptors (Fig. 24-10). 6 vasoconstrictor response. 11
ET is also a potent vasoconstrictor, which is stimulated by ADH, Renal compensation is triggered initially by a decrease in kid-
catecholamines, AT, and growth factors. Two ET receptor sites, ney perfusion, which decreases glomerular filtration rate (GFR)
ET-A and ET-B, have been identified. The ET-A elicits, in addi- and activates the RAAS, resulting in an increased SVR and in-
22
tion to peripheral vasoconstriction, an increase in inotropy, fluid creased sodium and water absorption. Under normal physiologic
retention, and growth or hypertrophy. The ET-B receptor is less conditions these pathways act in concert to maintain volume sta-
well understood, although it can mediate vasoconstriction and tus, vascular tone, and optimize cardiac output. However, chronic
also a vasodilator effect through increased levels of nitric oxide activation of these systems leads to worsening of the syndrome. 26
(NO) and prostaglandins. Plasma ET correlates directly with PA Mediators of the selective vasoconstrictor response include NE,
27
pressures and PA resistance and may play a role in pulmonary hy- ADH, AT, and ET. Aldosterone, a steroid hormone, increases tu-
pertension seen in patients with HF. 11 Counter-regulatory medi- bular sodium reabsorption along with AT and NE. ADH acts on
ators that cause vasodilatation include the natriuretic peptides, the collecting ducts to promote water reabsorption. In early HF,
NO, bradykinin, dopamine, and some of the prostaglandins, all catecholamine, ADH, and ET play the major role in stimulating
of which act directly to relax arteriolar smooth muscle. NO, a aldosterone secretion. 23 In patients with advanced HF, the most
free-radical gas initially known as endothelial-derived relaxing fac- important stimulus for aldosterone release is AT, whose levels are
tor, is synthesized by the vascular endothelium. Inability of the increased with diuretic therapy. 22
endothelium to respond to vasodilator stimulus of NO may con- Natriuretic peptides are counter-regulatory mediators pro-
tribute to the exercise intolerance in patients with HF. Bradykinin duced in the body. This family of peptides includes ANP, BNP,
and related peptides are vasodilators. Bradykinin is a substrate for and clearance natriuretic peptide (CNP). The heart itself produces
angiotensin-converting enzyme (ACE) that is also responsible for ANP and BNP. ANP is stored mainly in the right atria, and an in-
the production of AT. In addition, bradykinin also inhibits mal- crease in atrial distending pressure, however produced, leads to
adaptive growth. 6,7 Adrenomedullin is a peptide with vasodilating the release of ANP. BNP, identified initially in the brain, is syn-
and natriuretic properties. It also has positive inotropic effects. The thesized in the ventricles and is released in response to increased
clinical importance of these effects on HF is not fully established. 25 ventricular pressure. 27 CNP is produced in blood vessels and in
Dopamine, which is a precursor to NE, is a catecholamine that has the brain. CNP appears to act primarily as a clearance receptor
central and peripheral effects. At low concentrations, dopamine that regulates levels of the peptides and reduces vascular resistance