Regulation of intracellular pH in the stomach.
The following picture emerges from the relatively small literature concerned with pHi regulation in the stomach. Oxyntic cells have a H,K-ATPase at the luminal membrane and both Na+-H+ and Cl(-)-HCO3 exchangers at the serosal membrane. The intrinsic buffer capacity is 40-50 mM/pH. In the resting state, when the H, K-ATPase is inactive, pHi is 7.1. The Na+-H+ exchanger prevents acidic shifts of pHi, and the Cl(-)-HCO3 exchanger prevents alkaline shifts. The combined operation of the two appears to contribute directly to the net Cl- secretion (and short-circuit current) generated by resting OC. In the stimulated state, H+ secretion into the gland lumen via the H,K-ATPase increases, and Cl- movement across the serosal membrane via exchange for HCO3 doubles or triples; however, pHi remains roughly constant (delta pHi less than or equal to 0.1 units). The large increase in Cl- and HCO3 movement across the serosal membrane requires one (or all) of the following events: The anion exchanger changes its characteristics (Km or Vmax); [Cl-]i decreases; or other membrane mechanisms must be activated. Chief cells also have a pHi of 7.1 and a Bi of 40-50 mM/pH. They exhibit Na+-dependent and Cl(-)-dependent changes of pHi that are consistent with the presence of both Na+-H+ and Cl(-)-HCO3 exchangers. The Na+-dependent changes of pHi are larger and the Cl(-)-dependent changes are smaller in CC than in OC. Surface cells exhibit changes of AO fluorescence that indicate that there is a Na+-H+ exchanger and a HCO3 conductance. The H+ permeability of the luminal membranes of all cells is very low, while that of the serosal membrane (via the cation and anion exchangers) is high.
D000818:Animals; D005744:Gastric Acid / Q000502:physiology*; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D013276:Stomach Ulcer / Q000503:physiopathology