Neuroendocrine manifestations of congestive heart failure

Gary S. Francis

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37 Scopus citations


Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.

Original languageEnglish (US)
Pages (from-to)9A-13A
JournalThe American Journal of Cardiology
Issue number2
StatePublished - 1988

Bibliographical note

Funding Information:
From the Department of Medicine, Division of Cardiology,V eterans Administration Medical Center, Minneapolis, Minnesota. This study was supported by Grants HL22977-03 and HL07184 from the Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, and the Veterans AdministrationR esearch Service, Washington, D.C.

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