Modulation by calcium of the potassium permeability of dog heart sarcolemmal vesicles.

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Abstract
The movement of K+ in heart sarcolemmal vesicles was followed through the opposing movement of the tetraphenylphosphonium ion. Ca2+ (5-50 .mu.M) stimulates the efflux of K+ from K+-loaded vesicles [Km(Ca2+) .apprxeq. 10 .mu.M], 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 .mu.M Ca2+ [Km(Ca2+) .apprxeq. 10 .mu.M]. The Ca2+-induced increase of K+ permeability does not become spontaneously inactivated. The effects of some inhibitors were 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+ while quinidine (IC50 [mean inhibitory concentration] = 12 .mu.M) and trifluoperazine (IC50= 8 .mu.M at 50 .mu.g of sarcolemmal protein per ml) inhibit.