AJP - Gastrointestinal and Liver Physiology, Vol 261, Issue 1 111-G118, Copyright © 1991 by American Physiological Society

ARTICLES

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

S. I. Lee and R. J. Turner
Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.

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.

This article has been cited by other articles:

				M. A. Robertson, M. Woodside, J. K. Foskett, J. Orlowski, and S. Grinstein Muscarinic Agonists Induce Phosphorylation-independent Activation of the NHE-1 Isoform of the Na+/H+ Antiporter in Salivary Acinar Cells J. Biol. Chem., January 3, 1997; 272(1): 287 - 294. [Abstract] [Full Text] [PDF]