A muscarinic agonist-stimulated chloride efflux pathway is associated with fluid secretion in rat parotid acinar cells.
Cl- efflux from rat parotid acinar cells was stimulated by the muscarinic-cholinergic agonist carbachol (K0.5 approximately 1 microM). Carbachol application resulted in a rapid (T1/2 less than 10 sec.) and dramatic (approximately 50%) loss of intracellular Cl- followed by a much slower (T1/2 approximately 2 min) recovery to approximately 70% of original acinar Cl- content. Diphenylamine-2-carboxylate (1 mM), a putative Cl- channel blocker, blunted the initial Cl- loss and enhanced the subsequent recovery of Cl- content, while bumetanide (0.1 mM) blocked Cl- recovery with no effect on Cl- loss. Calculation of the rate of salivary secretion from measurements of sustained stimulated acinar Cl- release in vitro, yielded a value of 14 microliters/gland/min, in excellent agreement with previously published in vivo data. These results demonstrate that Cl- loss via this efflux pathway can account for fluid secretion from the rat parotid gland.
D000818:Animals; D001693:Biological Transport, Active; D002034:Bumetanide / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology*; D002712:Chlorides / Q000378:metabolism*; D006207:Half-Life; D008297:Male; D010306:Parotid Gland / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D062367:ortho-Aminobenzoates / Q000494:pharmacology
D002712:Chlorides; D062367:ortho-Aminobenzoates; D002034:Bumetanide; D002217:Carbachol; C001209:fenamic acid; D011188:Potassium