Neurohumoral control mechanisms in congestive heart failure.
Neurohumoral vasoconstrictor systems may play an important role in the hemodynamic derangement and natural history of congestive heart failure (CHF) by raising impedance to left ventricular ejection and shifting blood centrally to augment cardiac filling. Activation of the sympathetic nervous system, and renin-angiotensin system, and the antidiuretic hormone-vasopressin system can be demonstrated in clinical CHF by increased plasma levels of norepinephrine, renin activity, and arginine vasopressin. Because the magnitude of increase in each of these hormones varies widely from patient to patient, profiling of the neurohumoral response might provide new insight into the mechanisms of regulation of the circulation in CHF and into specific management with drugs to inhibit or reverse the vasoconstrictor process. Preliminary encouraging experience with converting-enzyme inhibitors to block formation of angiotensin II and alpha-receptor blockers to inhibit norepinephrine-induced vasoconstriction raise the possibility that selective therapy may eventually have a place in long-term management of CHF. Controlled trials in a larger patient population are now required.
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D018377:Neurotransmitter Agents / Q000502:physiology*; D012083:Renin / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014661:Vasoconstriction; D014665:Vasodilator Agents / Q000627:therapeutic use; D014667:Vasopressins / Q000502:physiology
D018377:Neurotransmitter Agents; D014665:Vasodilator Agents; D014667:Vasopressins; D000804:Angiotensin II; D012083:Renin