Cardiac and Baroreflex Control of the Circulation in Heart Failure

  • I. H. Zucker

Abstract

Neurohumoral abnormalities in heart failure include increased secretion of vasoactive hormones such as catecholamines [1], vasopressin [2,3], renin-angiotensin [4], and prostaglandins [5]. Alterations in autonomic function also occur in heart failure, especially as regards the arterial baroreflex control of heart rate [6–8]. It is generally assumed that the initial elevation in sympathetic tone that occurs in heart failure is mediated by unloading of the arterial baroreceptors due, in part, to a falling cardiac output. Although this idea fits with our current understanding of the reflex control of blood pressure, it is a simplification to think that the unloading of normally functioning reflexogenic areas of the circulation in a chronic disease state accounts for this observation. Heart failure results in an increase in catecholamine excretion and in plasma catechols [1,9], while at the same time specific organs such as the heart are depleted of catecholamines [10]. In addition, patients and experimental animals with heart failure are significantly hyporesponsive to administration of exogenous catecholamines [11–13]. This apparent paradox may have important implications in determining the mechanism(s) of the alterations in cardiovascular reflex function in heart failure.

Keywords

Depression Attenuation Prostaglandin Norepinephrine Epinephrine 

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© Springer-Verlag Berlin Heidelberg 1991

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  • I. H. Zucker

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