Depolarization-Stimulated 42K+ Efflux in Rat Aorta is Calcium- and Cellular Volume-Dependent

The purpose of this study was to investigate the factors controlling membrane permeability to potas-sium of smooth muscle cells from rat aorta stimulated by depolarization. The increase in 42K + efflux (change in the rate constant) induced by depolarization (application of high concentrations of potas-sium chloride) was inhibited significantly by the calcium antagonists diltiazem and nisoldipine. Parallel inhibitory effects on contraction were observed. Diltiazem also inhibited potassium-stimulat-ed 1(lCI ~ efflux. The addition of 25-150 mM KCI to normal physiologic solution stimulated 42K + efflux in a concentration-dependent manner. Diltiazem suppressed potassium-stimulated 42K+ efflux ap-proximately 90 % at 25 mM KCI and approximately 40 % at 150 mM KCI. The ability of nisoldipine to inhibit 42K + efflux also diminished as the potassium chloride concentration was elevated. The compo-nent of efflux that was resistant to calcium antagonists probably resulted from a decrease in the electrochemical gradient for potassium. Cellular water did not change during potassium addition. Substitution of 80 and 150 mM KCI for sodium chloride produced cellular swelling and enhanced potassium-stimulated 42K + efflux compared with potassium chloride addition. The addition of su-crose to prevent cellular swelling reduced efflux response to potassium substitution toward that of potassium addition. A hvpoosmolar physiologic solution produced an increase in the42K+ efflux and