Carbachol-induced potassium release in rat parotid acini: comparison of the roles of cytosolic Ca2+ and protein kinase C.

Carbachol (CCh) stimulated K+ release from rat parotid acini. Treatment with the intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) or the intracellular Ca2+ chelator 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) strongly suppressed the CCh-induced K+ release. Combined addition of the Ca2+ ionophore ionomycin and the microsomal Ca(2+)-ATPase inhibitor thapsigargin caused a rapid increase in cytosolic Ca2+ concentration ([Ca2+]i) and resulted in a marked release of K+. In the absence of extracellular Ca2+, CCh or a combination of ionomycin and thapsigargin caused a transient release of K+ which correlated well with the transient change in [Ca2+]i. On the other hand, phorbol 12-myristate 13-acetate (PMA) did not potentiate the CCh-induced K+ release, although the CCh-induced amylase release was significantly enhanced in the presence of PMA. Staurosporine, a protein kinase C-inhibitor, did not inhibit the CCh-induced K+ release, which was in contrast with its inhibitory effect on amylase release. These results suggest that the K+ release from rat parotid acini induced by CCh stimulation is mediated by a rapid increase in [Ca2+]i but is not associated with activation of protein kinase C. This signal pathway is different from that for amylase release where activation of protein kinase C plays an important role.