Structural cardiovascular adaptation and the consequences for baroreflexes.

Abstract

Changes in arterial baroreflex control of the circulation occur in experimental and in human hypertension. Hypertension can affect the afferent, the central, and the efferent portions of the baroreflex. Structural cardiovascular adaptation due to stiffening of the vascular wall is usually thought to influence the afferent component of the baroreflex, but it can also influence the effector component. Resetting of central mechanisms of the baroreflex also occurs. Cardiopulmonary baroreflexes appear to be enhanced in young spontaneously hypertensive rats (SHR) and in borderline hypertensive patients, probably because of reduced venous compliance that shifts blood to the cardiovascular compartments (atrium, ventricle) where the receptors are located. Progression of cardiac hypertrophy is likely to reverse this enhanced reflex activity. In hypertension the carotid sinus reflex appears to be readjusted in such a way as to protect against a further rise in blood pressure, rather than providing protection, as in normotension, against a fall in blood pressure. Thus the homeostatic functions of the reflex are maintained and readjusted to the needs of the hypertensive circulation. It is interesting to speculate that increased afferent inhibition from "volume" receptors in the cardiopulmonary area may represent a homeostatic attempt to buffer an early increase in sympathetic activity to the kidney.