Carbachol-Induced Potassium Release in Rat Parotid Acini: Comparison of the Roles of Cytosolic Ca²⁺ and Protein Kinase C

Abstract

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 Ca²⁺-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.