Effects of ion transport inhibition on rat mandibular gland secretion.

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 HCO3 from 14 +/- 0.9 mmol/L to 67 +/- 1.5 mmol/L. Furosemide (1 mmol/L), which blocks Na-K-2Cl symports and Cl-HCO3 antiports, had effects similar to those of gluconate replacement, except that secretion was reduced only by 59%. Bumetanide (1 mmol/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 HCO3 slightly. Ba (3 mmol/L), tetraethylammonium (10 mmol/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 mmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)