Arterial baroreceptors in the management of systemic hypertension

Abstract

Hypertension is a multifactorial disease associated with significant morbidity. Increased sympathetic nervous system activity has been noted as an important etiologic factor and is, in part, regulated by afferent input arising from arterial and cardiopulmonary baroreceptors, activation of which causes inhibition of sympathetic output. It was thought for many years that baroreceptors control only short-term blood pressure changes, a conclusion stemming from observations in sinoaortic denervation (SAD) animal models and the phenomenon of rapid baroreceptor resetting, also seen in animal models. Newer observations, however, indicate that SAD is rather imperfect and resetting is rarely complete. Recent studies reveal that baroreceptors control sympathetic output on a more long-term basis and participate in fluid volume regulation by the kidney, and thus have the potential to adjust blood pressure chronically. Importantly, these findings are consistent with studies and observations in humans. Meanwhile, a model of electrical stimulation of the carotid sinus has been developed and successfully tested in animals. Following these encouraging results human trials to evaluate the clinical application of electrical carotid sinus manipulation in the treatment of systemic hypertension have commenced, and results so far indicate that this represents an exciting potential tool in the clinician's armament against chronic arterial hypertension.<br />

Figure 1

A schematic representation of the complex function and multiple interactions among arterial baroreceptors, cardiovascular system and neural pathways. The main baroreceptor function consists of blood pressure regulation through a variety of mechanisms that include modification of the sympathetic output, loss of afferent baroreceptor stimulus in cases of baroreceptor denervation, baroreceptor resetting and possibly other mechanisms unknown at present. Changes of the vascular physiology due to aging, atherosclerosis, diet, or after carotid endarterectomy alter baroreceptor sensitivity that subsequently impacts blood pressure and heart rate control. Finally, heart rate changes due to fluctuations in the parasympathetic activity or altered response to vasoactive medications and overall baroreceptor sensitivity have an impact on the short- and long-term blood pressure regulation.

Figure 2

Long- and short-term blood pressure regulation by arterial baroreceptors. Loss of parasympathetic input as well as loss of afferent stimulus in cases of baroreceptor denervation results in an abrupt increase in the MAP. Baroreceptors then rapidly reset and the blood pressure returns to pre-denervation levels. However, baroreceptors participate in long-term blood regulation. Experimental evidence indicates that in cases of catecholamine secretion, volume overload or increased angiotensin II secretion, increased baroreceptor pathway activity is followed by diminished sympathetic output and pressure normalization.