The role of buffer anions and protons in secretion by the rabbit mandibular salivary gland.

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Abstract
The role of extracellular HCO3- and H+ in the formation of primary saliva and its subsequent modification by the glandular ducts was investigated in the isolated perfused mandibular salivary gland of the rabbit. Variation of extracellular HCO3- concentration between 12.5 and 50.0 mmol/l had no effect on salivary flow rate or on Na+ and K+ excretion, even though salivary HCO3- (and Cl-) content altered with changes in the extracellular concentration of the 2 anions. Complete replacement of perfusate HCO3- by Cl- reduced fluid secretion by 34% and almost abolished ductal Na+ absorption. When extracellular pH was controlled by replacing HCO3- with the hydrophilic HEPES [N-2-hydroxyethylpiperazine-N''-2-ethanesulfonic acid] buffer, fluid secretion but not ductal Na+ absorption was restored to normal. Complete replacement of exogenous HCO3- with acetate increased fluid secretion by 110% and also stimulated ductal Na+ absorption. This effect did not appear to be related to changes in cell pH and remains unexplained. Acetate entered the saliva in concentrations comparable to those seen for HCO3- in control experiments. Salivary secretion showed an almost linear dependence on extracellular pH, rising from 14% of control (pH 7.4) levels at pH 6.2 to 130% at pH 7.8. Ductal Na+ absorption showed a similar pH dependence. Carbonic anhydrase inhibitors did not affect fluid secretion rates (except when supramaximal doses of acetylcholine were used to evoke secretion) but they did cause a large reduction in salivary HCO3- output. In glands perfused with acetate rather than HCO3-, carbonic anhydrase inhibitors had no effect on excretion of fluid, acetate or metabolically derived HCO3-. The effect of the inhibitors on HCO3- output was probably at the site of primary secretion rather than at the ductal site of HCO3- transport.