Kinin receptors mediating the effect of bradykinin on gastric acid secretion.

Kinins, and bradykinin in particular, can affect electrolyte transport in different segments of the intestine, thus being able to stimulate chloride secretion. Since the stomach is the main chloride secretory unit in the gastrointestinal tract, we have investigated the effect of bradykinin on acid secretion in the isolated frog (Rana catesbeiana) gastric mucosa. Bradykinin [2 x 10(-8) to 2 x 10(-6) M] and des-Arg9-bradykinin [2 x 10(-9) to 2 x 10(-7) M] were able to stimulate acid secretion in a dose-dependent manner. The bradykinin [2 x 10(-7) M] and des-Arg9-bradykinin (2 x 10(-8) M]-induced acid secretion was unaffected by Thi5,8,D-Phe7-bradykinin [2 x 10(-7) to 2 x 10(-5) M], a B2-kinin receptor antagonist. Interestingly, the B1-kinin receptor antagonist, des-Arg9-(Leu8)-bradykinin [2 x 10(-7) to 2 x 10(-5) M] blocked both bradykinin- and des-Arg9-bradykinin-stimulated acid secretion. Although the kininase I inhibitor, D-L-mercapto-methyl-3-guanidino-ethyl-propanoic acid [2 x 10(-6) and 2 x 10(-5) M] had no effect on des-Arg9-bradykinin-induced acid secretion, it inhibited the response to bradykinin. We conclude that bradykinin requires, at least in part, hydrolysis to des-Arg9-bradykinin to increase gastric acid secretion and that its effect is mediated by B1-kinin receptors.