Baroreflexes in Congestive Heart Failure

Abstract

It has been known for many years that clinical congestive heart failure is accompanied by a neurohumoral excitatory state characterized by increased levels of norepinephrine and of muscle sympathetic nerve activity, plasma renin and vasopressin activity, increased circulating angiotensin II, and aldosterone. These neurohumoral mechanisms augment peripheral vasoconstriction and sodium retention by the kidney and are the hallmarks of clinical congestive heart failure. A similar neurohumoral excitatory state can be provoked in normal animals following acute interruption of sensory input from the arterial baroreceptors and from cardiac receptors with afferent vagal fibers [1]. We have previously suggested that the neurohumoral excitatory state could result in part from baroreflex abnormalities which may be present in congestive heart failure [2]. If this is so, then it is possible that such abnormalities could be present in the afferent limb of these reflexes, in the CNS, or in the neuroeffector mechanisms. Whether or not baroreflexes play an important causal role in the development of the neurohumoral excitatory rate, abnormalities of these reflexes still may be important in terms of interfering with the normal adaptive mechanisms for dealing with cardiovascular stresses to which humans are normally exposed. For example, exercise and emotion produce sympathoexcitation, tachycardia, and hypertension, which are modulated by baroreflex mechanisms.

Supported by HL30506 and by funds from the Veterans Administration. Dr. Dibner- Dunlap is a Research Associate Awardee of the Veterans Administration.