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The Neurohumoral Axis in Congestive Heart Failure

GARY S. FRANCIS, M.D.; STEVEN R. GOLDSMITH, M.D.; T. BARRY LEVINE, M.D.; MARIA TERESA OLIVARI, M.D.; and JAY N. COHN, M.D.
[+] Article and Author Information

Grant support: by grants HL22977-03 and HL07184 from the National Heart, Lung, and Blood Institute; and a grant from the Veterans Administration Research Service. *Dr. Goldsmith is the recipient of a Clinical Investigator Award from the National Institutes of Health.

▸Requests for reprints should be addressed to Gary S. Francis, M.D.; Cardiovascular Research (11 ICl), Veterans Administration Medical Center, 54th Street and 48th Avenue South; Minneapolis, MN 55417.


Minneapolis, Minnesota


© 1984 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1984;101(3):370-377. doi:10.7326/0003-4819-101-3-370
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The incidence of congestive heart failure is increasing in the United States. This common syndrome is characterized not only by impaired ventricular function but also by an increase in some endogenous vasoconstrictor substances, including norepinephrine, angiotensin II, and arginine vasopressin. Although activation of the systems that release these substances is presumed to be compensatory (to maintain perfusion pressure during inadequate flow), the sympathetic nervous system, renin-angiotensin-aldosterone system, and arginine vasopressin may contribute to the pathogenesis of the syndrome. The excessive vasoconstriction present in heart failure likely produces a further burden on the failing myocardium. New strategies in therapy are being developed to counteract the activation of vasoconstrictor forces in congestive heart failure. Data indicate that selective blockade of the reninangiotensin system is useful. Preliminary data suggest that inhibition of the sympathetic nervous system may be helpful, and inhibition of vasopressin in animals with heart failure is being studied. New and more selective therapy for heart failure may come from these studies.

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