Cardiac afferents and neurohormonal activation in congestive heart failure.

Abstract:

:Cardiac chambers have afferent connections to the brainstem and to the spinal cord. Vagal afferents mediate depressor responses and become activated by volume expansion, increased myocardial contractility and atrial natriuretic factor. Sympathetic afferents, on the contrary, are activated by metabolic mediators, myocardial ischemia and cardiac enlargement. These opposite behaviors may lead to activation or suppression of the sympathetic nervous system and of the renin-angiotensin-aldosterone system. As cardiac diseases progress, the heart dilates, plasma norepinephrine increases, atrial natriuretic factor is released and the renin-angiotensin-aldosterone system is suppressed to maintain water and sodium excretion. This dissociation of the neurohormonal profile of cardiac patients, may be explained by coactivation of sympathetic afferents, by cardiac dilatation, and of vagal afferents by atrial natriuretic factor. In more advanced stages, atrial natriuretic factor suppression of the renin-angiotensin-aldosterone system is overridden by overt sympathetic activation and sodium and water retention ensues. Digitalis, angiotensin-converting enzyme inhibitors and beta-blockers selectively decrease cardiac adrenergic drive. A common mechanism of action, to all three groups of drugs, would be attenuation of sympathetic afferents and partial normalization of vagal afferents. Consequently, heart size and cardiac afferents emerge as the key factors to understand the pathophysiology and treatment of the syndrome of congestive heart failure.

journal_name

Med Hypotheses

journal_title

Medical hypotheses

authors

Davila DF,Donis JH,Bellabarba G,Torres A,Casado J,Mazzei de Davila C

doi

10.1054/mehy.1999.0029

keywords:

subject

Has Abstract

pub_date

2000-02-01 00:00:00

pages

242-53

issue

2

eissn

0306-9877

issn

1532-2777

pii

S0306-9877(99)90029-4

journal_volume

54

pub_type

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