Effects of Ion Transport Inhibition on Rat Mandibular Gland Secretion

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Abstract
The effects of substituting gluconate for extracellular Cl, and of treatment with various ion transport blockers, on cytosol pH (pHi) and secretion by the acetylcholine stimulated rat mandibular gland were studied in vitro. Gluconate replacement increased pHi from 7.12 ± 0.02 to 7.27 ± 0.04, caused secretory rate to fall by 75%, and increased salivary HC03 from 14 ± 0.9 mmollL to 67 ± 1.5 mmoll L. Furosemide (I mmol/L), which blocks Na-K-2Cl symports and Cl-HCO 3 antiports, had effects similar to those of gluconate replacement, except that secretion was reduced only by 59%. Bumetanide (1 mmoll L), which blocks only Na-K-2Cl symports, caused a 67% reduction in secretion rate, but it had little effect on pHi and caused only a small rise in salivary HCO3 concentration. SITS (1 mmol/L), which blocks Cl-HCO3 antiports, increased pHi to 7.26 ± 0.03 and induced a small rise in the secretory rate. Methazolamide and acetazolamide (1 mmol/L), both of which inhibit carbonic anhydrase and may also block anion channels, increased pHi to 7.43 ± 0.02 and 7.20 ± 0.03, respectively, but had no effect on secretory rate, and reduced salivary HC03 slightly. Ba (3 mmol/L), tetraethylammonium (10 mmoll L), and decamethonium (5 mmol/L) all caused marked but reversible reductions in secretory rate, consistent with the known actions of these agents on K channels. Ba, however, also appeared to act as a Ca antagonist, an action that it seemed to share with Mn ions (5 mmoll L). The results are interpreted in terms of a secretion model based on the presence, in the baso-lateral plasma membranes of the secretory cells, not only of a Na-K-2Cl symport, but also of Na-H and Cl-HC03 antiports, contributing, respectively, to secretion in the proportions 8:5:3.

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