Regulation of murine acid secretion by CO2.

To determine whether endogenous metabolic sources alone provide sufficient CO2 for acid secretion in mammals, basal and stimulated acid secretion and metabolic CO2 production were measured concurrently in mouse stomachs, in vitro, without exogenous CO2, and after addition of 5% CO2 serosally. Basal acid secretion was varied by changing luminal pH from 3.2 to 4.0. In the absence of an exogenous supply of CO2 acid secretion was stable under basal conditions and increased during cholinergic stimulation with carbachol. Serosal CO2 supply increased basal and stimulated acid secretion. The increase in basal acid secretion depended on the initial level of acid secretion. At pH 4.0, exogenous CO2 increased acid output (mean +/- SD) by 13% from 112 +/- 11 nmol/min to 126 +/- 8 nmol/min (P < 0.03), whereas at pH 3.6 the increase was 40% (63 +/- 14 to 88 +/- 20 nmol/min, P < 0.04) and 157% at pH 3.2 (21 +/- 13 to 54 +/- 14 nmol/min, P < 0.002). Following cholinergic stimulation a maximal acid output of 321 +/- 38 nmol/min was attained without serosal CO2, whilst addition of 5% CO2 to the serosal solution increased maximal acid secretion by 49% to 479 +/- 96 nmol/min (P < 0.005). Metabolic activity, measured as total gastric CO2 production, was greater as acid secretion rates increased [239 +/- 20 nmol/min at 21 +/- 13 nmol/min (luminal pH 3.2) versus 406 +/- 28 nmol/min at 321 +/- 17 nmol/min (after cholinergic stimulation)]. The data support the concept that basal and sub-maximal acid secretion can be maintained by CO2 available from metabolic sources, but full expression of the acid secretory apparatus requires exogenous CO2.