Is resting state HCO3‐ secretion in frog gastric fundus mucosa mediated by apical Cl(‐)‐HCO3‐ exchange?

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Abstract
1. We have tested the widely accepted hypothesis that resting‐state bicarbonate secretion of gastric fundus mucosa is mediated by Cl(‐)‐HCO3‐ exchange in the apical membrane of surface epithelial cells (SECs). To this end, SECs of isolated fundus mucosa of Rana esculenta were punctured with double‐barrelled microelectrodes to measure intracellular pH (pHi). 2. No significant pHi changes were observed in response to changing luminal HCO3‐ and/or Cl‐ concentrations. The change in pHi (delta pHi) in response to luminal chloride substitution averaged 0.00 +/‐ 0.01 pH units (mean +/‐ S.E.M.; n = 48), and did not change after blocking putative basolateral acid/base transporters which could have masked the pHi response. 3. On the other hand, pHi responded readily and reversibly to luminal perfusion with either low‐pH (pH 2.5) solution (delta pHi = ‐0.36 +/‐ 0.05; n = 4; P < 0.01) or CO2‐free HCO3‐ Ringer solution (delta pHi = +0.10 +/‐ 0.01; n = 29; P < 0.001). These observations demonstrate that the solution change was effective and complete within 1 min and show that the apical membrane of SECs is permeable to CO2. 4. The apical membrane of frog SECs could not be stained with an antibody against the C‐terminal end of the mouse Cl(‐)‐HCO3‐ exchanger isoform AE2, although this antibody readily stained the basolateral membrane of the oxyntopeptic cells (OCs). 5. In conclusion, the presence of a Cl(‐)‐HCO3‐ exchanger in the apical membrane of SECs of frog gastric fundus mucosa in the resting state could not be confirmed, but other models of HCO3‐ secretion cannot be fully excluded. Observations from electrical measurements, favouring a model of conductive HCO3‐ secretion, point to the OCs rather than the SECs as a site of origin of HCO3‐ secretion.

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