Endothelium-dependent increases in rat gastric mucosal hemodynamics induced by acetylcholine and vagal stimulation.

The role of vascular endothelial cells in the vagal control of hemodynamics was studied in rat gastric mucosa. Vagal stimulation and intra-arterial administration of acetylcholine and of papaverine increased hemoglobin (Hb) and oxygen saturation of hemoglobin (SO2) in the gastric mucosa. The increases induced by vagal stimulation were reduced but not abolished by atropine. The responses to acetylcholine and vagal stimulation were reduced by quinacrine, p-bromophenacyl bromide and nordihydroguaiaretic acid, while indomethacin had no effect. Intra-arterial infusion of collagenase removed the endothelial cells from submucosal vasculatures and depressed the increase in mucosal hemodynamics in response to acetylcholine and vagal stimulation. The response to papaverine was not depressed in rats treated with quinacrine or collagenase. These results suggest that the increase in gastric mucosal blood flow induced by acetylcholine or vagal stimulation is mediated by the endothelium-derived relaxing factor.