PROTECTION BY CAPSAICIN AGAINST ATTENUATED ENDOTHELIUM-DEPENDENT VASORELAXATION DUE TO LYSOPHOSPHATIDYLCHOLINE

Previous studies have shown that pretreatment with calcitonin gene-rel ated peptide (CGRP), a principal transmitter in sensory nerves, can pr otect the endothelial cell. We therefore evaluated whether in vivo cap saicin treatment prevents endothelial damage elicited by lysophosphati dylcholine (LPC) in the rat aorta. Acute treatment or repeated pretrea tment with capsaicin resulted in stimulation of neurotransmitter relea se from sensory nerves or depletion of their transmitter content respe ctively. Vasodilator responses to acetylcholine (ACh) were examined in the aorta of these animals. Acute application of capsaicin (50 mg/kg) increased the plasma concentration of CGRP-like immunoreactivity (CGR P-LI) concomitantly with a reversal of the inhibition by LPC of endoth elium-dependent ACh-induced relaxation in the isolated rat aorta. Afte r repeated pretreatment with capsaicin to deplete sensory nerve neurot ransmitter content the effects of capsaicin were absent as shown by th e plasma CGRP-LI concentration and the vasodilator response to ACh. Th e results demonstrate that systemic capsaicin treatment, which evokes the release of CGRP from sensory nerves, protects the endothelial cell . The present study also suggests that CGRP may be an endogenous vascu lar protective substance.