Carbachol (CCh) stimulated K
+ release from rat parotid acini. Treatment with the intracellular Ca
2+ antagonist 8-(
N,
N-diethylamino)octyl-3, 4, 5-trimethoxybenzoate (TMB-8) or the intracellular Ca
2+ 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 Ca
2+ ionophore ionomycin and the microsomal Ca
2+-ATPase inhibitor thapsigargin caused a rapid increase in cytosolic Ca
2+ concentration ([Ca
2+]
i) and resulted in a marked release of K
+. In the absence of extracellular Ca
2+, CCh or a combination of ionomycin and thapsigargin caused a transient release of K
+ which correlated well with the transient change in [Ca
2+]
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 [Ca
2+]
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.
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