Nitric oxide mediates rat mucosal vasodilatation induced by intragastric capsaicin.

The role of endogenous nitric oxide (NO) in the gastric mucosal vasodilatation induced by acute intragastric perfusion with capsaicin or close-arterial infusion of rat alpha-calcitonin gene-related peptide (CGRP) was evaluated in the pentobarbitone-anaesthetised rat using laser Doppler flowmetry (LDF). The mucosal vasodilatation induced by intraluminal capsaicin (160 microM) was dose dependently reduced by the inhibitor of NO synthesis, NG-nitro-L-arginine methyl ester (L-NAME; 1-5 mg kg-1 i.v.), effects reversed by concurrent administration of L-arginine (100 mg kg-1 i.v.). L-NAME (2 mg kg-1) induced a small reduction in the mucosal vasodilatation induced by close-arterial infusion of rat alpha-CGRP (50 pmol kg-1 min-1). These findings indicate a role of NO in the gastric vasodilatation induced by stimulation of sensory neurones with intragastric capsaicin.