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 submaximal acid secretion can be maintained by CO₂ available from metabolic sources, but full expression of the acid secretory apparatus requires exogenous CO₂.