Secretagogue-induced 86Rb+ efflux from bovine parotid is HCO3- dependent.
Muscarinic agonist (carbachol)-induced K+ loss from a bovine parotid mince was studied using 86Rb+ as a K+ marker. In contrast to our previous studies with the rat parotid [Am. J. Physiol. 261 (Gastrointest. Liver Physiol. 24): G111-G118, 1991] in which both Cl(-)-dependent and HCO3(-)-dependent components of carbachol-induced 86Rb+ efflux were observed, no significant evidence for Cl(-)-dependent 86Rb+ loss was detected in the bovine parotid. HCO3(-)-dependent agonist-induced 86Rb+ loss was blunted by K+ and Cl- channel blockers and by removal of extracellular Ca2+, consistent with the hypothesis that this 86Rb+ loss occurs via a Ca(2+)-activated K+ channel and that this cation loss serves to electrically balance the concomitant loss of HCO3- via an electrically conductive pathway, presumably an apical anion channel. Acetate, formate, and propionate could substitute for HCO3-. Interpreted in terms of current models of salivary fluid secretion, which hypothesize that the production of fluid is secondary to anion secretion accompanied by an electrically coupled K+ loss, these results indicate that salivary production in the bovine parotid is driven almost exclusively by acinar HCO3- secretion.
Lee
S I
SI
Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
Turner
R J
RJ
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D002417:Cattle; D002712:Chlorides / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D010277:Parasympathomimetics / Q000494:pharmacology; D010306:Parotid Gland / Q000378:metabolism*; D012413:Rubidium / Q000378:metabolism*; D012414:Rubidium Radioisotopes; D012463:Saliva / Q000378:metabolism; D013268:Stimulation, Chemical
D001639:Bicarbonates; D002712:Chlorides; D010277:Parasympathomimetics; D012414:Rubidium Radioisotopes; D002217:Carbachol; D012413:Rubidium