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.