Thus our results show that the TRPV1, possibly via triggering release of SP which activates the NK1 and stimulates the sympathetic axis, plays a protective role against endotoxin-induced hypotension and mortality, suggesting that TRPV1 receptors are essential in protecting vital organ perfusion and survival during the endotoxic condition.
The most sensitive sites where application of SP into the NTS evoked dose-dependent hypotension and bradycardia were at the level of the posterior tip of the area postrema (zero level) and at the level of the obex.