Modulation by calcium of the potassium permeability of dog heart sarcolemmal vesicles.
The movement of K+ in heart sarcolemmal vesicles has been followed through the opposing movement of the tetraphenylphosphonium ion. Ca2+ (5-50 microM) stimulates the efflux of K+ from K+-loaded vesicles [Km(Ca2+) approximately equal to 10 microM]. and the activation requires that Ca2+ be present inside the vesicles together with K+. The efflux of 86Rb+ from K+-, Rb+-loaded vesicles is similarly stimulated by 5-50 microM Ca2+ [Km(Ca2+) approximately equal to 10 microM]. The Ca2+-induced increase of K+ permeability does not become spontaneously inactivated. The effects of some inhibitors have been tested under conditions in which Ca2+ promotes the entry of K+ into vesicles. In this system, direct interaction of the drug with the Ca2+ and K+ membrane binding site(s) was therefore studied. Tetraethylammonium ion, which inhibits the potential-dependent K+ channel, does not interfere with the effect of Ca2+ whereas quinidine (IC50 = 12 microM) and trifluoperazine (IC50 = 8 microM at 50 micrograms of sarcolemmal protein per ml) inhibit.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D004285:Dogs; D007202:Indicators and Reagents; D007700:Kinetics; D009206:Myocardium / Q000378:metabolism*; D009861:Onium Compounds / Q000378:metabolism; D009943:Organophosphorus Compounds; D010539:Permeability; D011188:Potassium / Q000378:metabolism*; D012508:Sarcolemma / Q000187:drug effects / Q000378:metabolism*
D007202:Indicators and Reagents; D009861:Onium Compounds; D009943:Organophosphorus Compounds; D011188:Potassium; D002118:Calcium; C013289:tetraphenylphosphonium