Calmodulin-dependent regulation of calcium-activated outward current in frog atrial membrane.
The steady-state outward current underlying the inward-going rectification in frog atrial fibers has been studied by the double sucrose gap technique. Similar to the case in sheep Purkinje fibers (18,19), the inward rectifying potassium channels in frog atrium are blocked by cesium (5 mM) and activated by increasing cytosolic calcium concentration (replacing 30% of the Na by sucrose). It was shown that trifluoperazine (5 x 10(-6) M), a widely used blocker of the Ca-calmodulin complex, inhibits the inward rectifying potassium channels. Diphenylhydantoin (5 x 10(-6) M), a putative inhibitor of Ca-calmodulin-mediated membrane phosphorylation produces a similar action. The inhibitory action of both blockers is not manifested after preliminary Cs+ (5 mM) exposure. The data obtained suggest that calcium activates the inward rectifying potassium channels in frog atrial fibers via Ca-calmodulin regulatory phosphorylation of the membrane proteins.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002147:Calmodulin / Q000378:metabolism*; D004562:Electrocardiography; D006325:Heart Atria / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism*; D009200:Myocardial Contraction / Q000187:drug effects; D010672:Phenytoin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011895:Rana ridibunda; D014268:Trifluoperazine / Q000494:pharmacology
D002135:Calcium-Binding Proteins; D002147:Calmodulin; D007473:Ion Channels; D014268:Trifluoperazine; D010672:Phenytoin; D011188:Potassium; D002118:Calcium