pH-sensitive anion exchanger in rat lacrimal acinar cells.

Basolateral membranes from rat lacrimal acinar cells contain Na(+)-H+ and Cl(-)-HCO3- antiport activities [Invest. Ophthalmol. Visual Sci. 28: 1726-1729, 1989; Am. J. Physiol. 255 (Gastrointest. Liver Physiol. 18): G367-G373, 1988]. This study evaluated factors involved in coupling ion fluxes through these antiporters. 22Na+ flux into acini isolated from rat exorbital glands was 94 +/- 6 nmol.mg-1.min-1, and it was accelerated threefold by 10(-5) M carbachol; neither resting nor stimulated influx was affected by bumetanide. It is, therefore, likely that a portion of the carbachol-dependent Na+ influx is mediated by Na(+)-H+ antiporters. 36Cl- flux into Cl(-)-loaded, unstimulated acini was 275 +/- 21 nmol.mg-1.min-1; Cl- flux into HCO3(-)-loaded acini was 204 +/- 2; Cl- flux into acini loaded with both Cl- and HCO3- was 253 +/- 32; and influx in the absence of exchangeable intracellular anions was 176 +/- 13. Therefore, Cl(-)-Cl- self-exchange represented the major component of anion exchanger-mediated Cl- flux into resting cells. As pHi was increased above 7.2 by potassium-nigericin pH clamping, Cl- fluxes into Cl(-)- and HCO3(-)-containing acini, but not into Cl(-)-depleted acini, were significantly accelerated. SITS completely abolished the pHi-activated increment of Cl(-)-Cl- exchange. Carbachol increased Cl- unidirectional flux into Cl(-)-loaded cells by 25% (P less than 0.1), apparently as a result of Na(+)-H+ antiporter-mediated cytoplasmic alkalinization.(ABSTRACT TRUNCATED AT 250 WORDS)