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Abstract
The change in the endothelial function by the application of 0.6 N HC1 and the effects of endothelium-derived relaxing factor (EDRF) inhibitors and nitrites on HC1-induced lesions were studied to clarify the effect of EDRF on gastric lesions in rats. The EDRF-induced increase in the gastric mucosal hemodynamics induced by vagal stimulation or intra-arterial administration of acetylcholine was inhibited by the EDRF inhibitors or removal of endothelial cells. Topical application of 0.6 N HC1 on the exposed gastric mucosa abolished the response of the mucosal hemodynamics to acetylcholine or vagal stimulation. Gastric lesions induced by 0.45 N HC1 were enhanced by EDRF inhibitors or removal of endothelial cells from gastric submucosal arterioles.