Paracrine role of prostanoids in activation of arterial baroreceptors: an overview

Abstract

Baroreceptors located in carotid sinuses and aortic arch are activated with increases in arterial pressure. The increased afferent nerve activity triggers reflex adjustments that buffer the rise in pressure. Mechanical deformation of baroreceptor nerve endings is considered the primary mechanism of receptor activation. Recent studies in our laboratory have demonstrated that prostanoids, most likely released from endothelial cells during stretch, contribute--as paracrine factors--to the activation of baroreceptors. Exposure of the isolated carotid sinus in anesthetized rabbits to prostacyclin (PGI2) or arachidonic acid increases baroreceptor sensitivity whereas inhibition of endogenous formation of prostanoids with indomethacin or aspirin decreases sensitivity. Baroreceptor sensitivity is also decreased after endothelial denudation and restored after adding PGI2 back to the denuded sinus suggesting that endothelium is the source of prostanoids that sensitize baroreceptors. Pathologic states such as chronic hypertension and atherosclerosis are associated with both endothelial cell dysfunction and decreased baroreceptor sensitivity. The endothelial cell dysfunction and impairment of prostanoid formation contribute to the decreased baroreceptor sensitivity in these diseases.