Intragastric pH regulates conversion from net acid to net alkaline secretion by the rat stomach

Our previous report showed gastric mucosal surface pH was determined by alk ali secretion at intragastric luminal pH 3 but by acid secretion at intraga stric pH 5. Here, we question whether regulation of mucosal surface pH is d ue to the effect of luminal pH on net acid/base secretions of the whole sto mach. Anesthetized rats with a gastric cannula were used, the stomach lumen was perfused with weakly buffered saline, and gastric secretion was detect ed in the gastric effluent with 1) a flow-through pH electrode and 2) a flu orescent pH-sensitive dye (Cl-NERF). During pH 5 luminal perfusion, both pH sensors reported the gastric effluent was acidic (pH 4.79). After perfusio n was stopped transiently (stop-flow), net acid accumulation was observed i n the effluent when perfusion was restarted (peak change to pH 4.1-4.3). Du ring pH 3 luminal perfusion, both pH sensors reported gastric effluent was close to perfusate pH (3.0-3.1), but net alkali accumulation was detected a t both pH sensors after stop-flow (peak pH 3.3). Buffering capacity of gast ric effluents was used to calculate net acid/alkaline secretions. Omeprazol e blocked acid secretion during pH 5 perfusion and amplified net alkali sec retion during pH 3 perfusion. Pentagastrin elicited net acid secretion unde r both luminal pH conditions, an effect antagonized by somatostatin. We con clude that in the basal condition, the rat stomach was acid secretory at lu minal pH 5 but alkaline secretory at luminal pH 3.