Figure 2.

Schematic representation of the tri-phasic capsaicin effect on blood pressure in experimental animals, along with the presumptive underlying molecular mechanisms of action (Figure courtesy of Attila Tóth). (A) When injected intravenously, capsaicin (CPS) evokes the Bezold–Jarisch reflex (green line); this produces a rapidly developing, but transient drop in blood pressure. The Bezold–Jarisch reflex is now thought to originate from cardiac inhibitory mechanoreceptors located in the left ventricle of the heart. The efferent reflex pathway, that runs in the vagal nerve, increases the parasympathetic tone. (B) Circulating capsaicin binds to TRPV1 receptors expressed on vascular smooth muscle (red line). This evokes a direct vasoconstrictive effect by allowing Ca²⁺ influx, increasing the blood pressure. (C) The molecular mechanism underlying the late drop in blood pressure (yellow arrow) is yet to be elucidated. To some extent, this may reflect a rebound effect that follows the disappearance of the myogenic tone. Alternative mechanisms include the CGRP effect (released from sensory afferents) on the vasculature and/or direct capsaicin action on endothelial cells.