Escape of gastric submucosal arterioles from acetylcholine-induced dilatation.

Escape from acetylcholine-induced dilatation of gastric submucosal arterioles was studied using in vivo microscopy in rats. Acetylcholine, physostigmine and atropine were applied topically to the submucosa. Experiments were videotaped and diameter changes of the submucosal arterioles were measured with an image splitting technique on playback of the videotapes. Acetylcholine, 10(-6) M and 10(-5) M, caused prompt dilatation of arterioles in a dose-dependent manner, and the dilatation was rapidly followed by escape (return of vessel diameter toward basal diameter in spite of the continued presence of acetylcholine). The escape from acetylcholine-induced dilatation was prevented by physostigmine in a dose-dependent manner, 10(-2) M completely inhibiting the escape. Physostigmine, by itself, 10(-4) M to 10(-2) M, dilated arterioles dose-dependently, and this dilatation was inhibited by atropine. These results indicate that escape of gastric submucosal arterioles from acetylcholine-induced dilatation is mediated by endogenous cholinesterase (catabolism of acetylcholine by endogenous cholinesterase), and basal arteriolar diameter may be determined, in part, by endogenous acetylcholine, this effect being modulated by endogenous cholinesterase.