Mechanism of secretagogue-induced HCO3- and Cl- loss from rat parotid acini.

The Cl(-)- and HCO3(-)-dependent components of muscarinic agonist (carbachol)-induced K+ loss from a rat parotid mince were studied using 86Rb+ as a K+ marker. Both components of 86Rb+ loss were blunted by K+ and Cl- channel blockers and by removal of extracellular Ca2+, consistent with the hypothesis that 86Rb+ loss occurs via a Ca(2+)-activated K+ channel and that this cation loss serves to electrically balance a concomitant loss of the corresponding anion via one or more conductive pathways (channels). Two tissue "pools" of 86Rb+ were observed, a carbachol-sensitive pool and a carbachol-insensitive pool (approximately 70 and approximately 30% of the total 86Rb+ content, respectively). There was no evidence for a time-dependent desensitization of the muscarinic response of the carbachol-sensitive pool. Cl(-)-dependent 86Rb+ loss was not affected by HCO3- addition, suggesting that both Cl- and HCO3- secretion are accompanied by 86Rb+ loss from the same pool and thus occur from the same cells. HCO3(-)-dependent 86Rb+ loss was not enhanced by lowering the extracellular Na+ concentration, indicating that the HCO3- exit pathway is not a Na(+)-HCO3- symport. The data are consistent with the postulate that Cl- and HCO3- are secreted by rat parotid acinar cells via the same or very similar conductive transport pathways in response to muscarinic stimulation.