Calcium-dependent K+ efflux from rat submandibular gland. The effects of trifluoperazine and quinidine.
The Ca2+-dependent K+ efflux from rat submandibular gland was studied using a K+-sensitive electrode. A K+ efflux was induced by either adrenalin or by using the divalent cation ionophore A23187 plus added Ca2+ to bypass the receptor mechanism. Trifluoperazine, which was used to investigate the role of calmodulin, was found to block the adrenalin-induced K+ efflux but not the A23187/Ca2+-induced K+ efflux. The adrenalin-induced K+ efflux was abolished by quinidine and the A23187/Ca2+-induced K+ efflux was significantly reduced by quinidine. In other experiments, the presence of indomethacin did not inhibit the adrenalin-induced K+ efflux, and exogenously added arachidonic acid did not induce a K+ efflux. It is concluded that neither prostaglandin synthesis, nor a cytosolic Ca2+-calmodulin complex is involved in the agonist-induced K+ efflux from rat submandibular gland. A similarity between the Ca2+-dependent K+ efflux mechanism of erythrocyte ghosts and submandibular tissue is indicated by their common response to quinidine.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D007700:Kinetics; D011188:Potassium / Q000378:metabolism*; D011802:Quinidine / Q000494:pharmacology*; D051381:Rats; D013363:Submandibular Gland / Q000187:drug effects / Q000378:metabolism*; D014268:Trifluoperazine / Q000494:pharmacology*
D014268:Trifluoperazine; D000001:Calcimycin; D011802:Quinidine; D011188:Potassium; D002118:Calcium; D004837:Epinephrine