Abstract
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 α-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 μM) was dose dependently reduced by the inhibitor of NO synthesis, N G-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 α-CGRP (50 pmol kg −1). These findings indicate a role of NO in the gastric vasodilatation induced by stimulation of sensory neurones with intragastric capsaicin.
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