Na+ transport properties of isolated rat parotid acini.

The effect of carbachol stimulation on the Na+ transport properties of rat parotid acini was characterized. Upon stimulation, the acinar Na+ concentration increased from 20 to 70 mM within 25 s, whereafter a backregulation toward the prestimulatory level was observed, mediated by the Na(+)-K+ pump. The transport mechanisms responsible for the net Na+ uptake observed between 10 and 20 s after carbachol stimulation in a Krebs-Ringer-bicarbonate medium (KRB) consisted of a dimethylamiloride-sensitive Na(+)-H+ exchange system (3.5 mmol.liter cell water-1.s-1 or approximately 75% of the total Na+ influx) and a bumetanide-sensitive cotransport system (of approximately 15%). The data are consistent with the residual influx being mediated by amiloride-sensitive Na+ channels. In unstimulated acini acidified by a NH4+ prepulse technique, the relationship between intracellular pH (pHi) and the rate of acinar Na(+)-H+ exchange was determined. At pHi 6.5 the rate of Na(+)-H+ exchange in a KRB medium amounted to 1.2 mmol.liter cell water-1.s-1 and ceased when pHi had recovered to 7.2. It was concluded that under physiological conditions carbachol stimulation activates Na(+)-H+ exchange, an effect that is responsible for the major part of the Na+ gain after stimulation. The role of cotransport in mediating net Cl- uptake against an electrochemical gradient was investigated. It was found that when the Na+ gradient is strongly reduced (in a 20 mM Na+ medium) a Cl(-)-HCO3- exchange system can mediate a net Cl- uptake at a rate similar to the rate observed in a medium containing high Na+. The results are compatible with both Cl(-)-HCO3- exchange and cotransport keeping an intracellular Cl- concentration above the electrochemical equilibrium under physiological conditions.