[Mechanisms of renal retention of sodium and water in heart failure, cirrhosis and pregnancy].

A decade after a unifying hypothesis of sodium and water regulation had been proposed, evidence has accumulated in support of common (patho)physiologic mechanisms of sodium and water retention in congestive heart failure, cirrhosis and pregnancy. Either primary arterial vasodilatation (cirrhosis, pregnancy), or a decrease in cardiac output (low-output heart failure) impair arterial circulatory integrity ("effective arterial blood volume"), which unloads ventricular and arterial baroreceptors. Consequently, activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, arginine-vasopressin, as well as other less well explored mechanisms occurs in an attempt to restore the arterial circulatory integrity. Consequences of this neurohumoral activation with arterial uderfilling include renal sodium and water retention and an increase in peripheral vascular resistance. In this review specific pathophysiologic mechanisms underlying the sodium and water retention in congestive heart failure, cirrhosis and pregnancy will be discussed.