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A rterial baroreceptors located in the carotid si/ \ nuses and aortic arch play a major role in A. \ control of circulation and regulation of arterial pressure. Increased arterial pressure triggers increased frequency of baroreceptor discharge, which leads to reflex adjustments that buffer the rise in pressure. It is established that baroreceptors are not activated by increases in arterial pressure directly but instead are activated by the increased vascular stretch or strain that accompanies the rise in pressure. Mechanical deformation of the baroreceptor nerve endings is usually considered the primary or even the sole determinant of the frequency of baroreceptor discharge. Are there other factors besides deformation that are important in activation of baroreceptors? In this issue of Hypertension, Wang et al report that exposure of the vascularly isolated carotid sinus in anesthetized dogs to the hormone aldosterone suppresses activation of baroreceptors without a change in vascular stretch as measured with sonomicrometer crystals. What is the mechanism of aldosterone-induced suppression of baroreceptor activity? Wang et al demonstrate that the inhibitory effect of aldosterone is dependent on the presence of intact endothelium and is blocked by the aldosterone receptor antagonist spironolactone. The simplest scenario is that aldosterone binds to its receptor in endothelial cells and alters the release of a diffusable mediator that acts directly on baroreceptor neurons to modulate their sensitivity. This study is the first to show that aldosterone modulates baroreceptor activity and adds to the growing evidence that humoral and endothelial factors modulate to a significant extent the sensitivity of baroreceptors.

hypertension

Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.