Cardiac and Baroreflex Control of the Circulation in Heart Failure

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.

Supported, in part, by NIH Grant Nos. HL 33359, HL 22594, and HL 38690.