title: 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 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.
authors.affiliation: Department of Dental Pharmacology, School of Dentistry, Higashi Nippon Gakuen University, Hokkaido.
authors.forename: Y
authors.initials: Y
authors.lastname: Tojyo
authors.forename: A
authors.initials: A
authors.lastname: Tanimura
authors.forename: S
authors.initials: S
authors.lastname: Matsui
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumoto
mesh_terms: D000470:Alkaloids / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology*; D003600:Cytosol / Q000378:metabolism; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004789:Enzyme Activation; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D015759:Ionomycin / Q000494:pharmacology; D008297:Male; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D019311:Staurosporine; D013729:Terpenes / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D019284:Thapsigargin
chemical_list: D000470:Alkaloids; D002121:Calcium Channel Blockers; D013729:Terpenes; D004533:Egtazic Acid; D015759:Ionomycin; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D019284:Thapsigargin; D002217:Carbachol; D011493:Protein Kinase C; D000681:Amylases; D019311:Staurosporine; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D013755:Tetradecanoylphorbol Acetate; D011188:Potassium; D002118:Calcium