Intracellular pH in the rat mandibular salivary gland: the role of Na-H and Cl-HCO3 antiports in secretion.

Intracellular pH (pHi) in the perfused rat mandibular gland was determined from the distribution of DMO (5,5-dimethyl-2,4-oxazolidinedione). In unstimulated glands, pHi averaged 7.12 +/- 0.02. Stimulation with a "standard" (submaximal) concentration (0.3 mumol/l) of acetylcholine (ACh) caused a fall in pHi to 6.81 +/- 0.06 over 60 min, but a maximal concentration (1.0 mumol/l) caused an initial rise in pHi to 7.60 +/- 0.02, followed by a fall to 7.45 +/- 0.02 over 60 min. After replacement of perfusate Cl with gluconate, the standard ACh concentration caused a rise in pHi to 7.50 +/- 0.02 followed by a fall to 7.27 +/- 0.04 after 60 min, concomitant with a 76% fall in secretory rate and a rise in salivary HCO3 concentration from 14 +/- 0.9 to 67 +/- 1.5 mmol/l. Furosemide (1 mmol/l) had a similar effect to gluconate replacement except that secretory rate fell only by 60%. Bumetanide (1 mmol/l), which inhibited secretion by 67%, did not cause pHi to rise following ACh stimulation but prevented the fall seen with ACh alone. Acetazolamide and methazolamide (1 mmol/l) had no effect on the salivary secretory response to ACh but they caused pHi to rise, respectively, to 7.20 +/- 0.03 and 7.43 +/- 0.02. Bumetanide and methazolamide together caused pHi to rise to 7.58 +/- 0.02 and reduced the secretory response to ACh by 91%. The disulfonic stilbene, SITS, caused pHi to rise to 7.26 +/- 0.03. Ouabain and amiloride both caused resting pHi to fall closer to equilibrium and largely abolished the gland's responsiveness to ACh.(ABSTRACT TRUNCATED AT 250 WORDS)