KCl depolarization increases Ca2+ sensitivity of contractile elements in coronary arterial smooth muscle.

The effects of KCl depolarization on the Ca2+ sensitivity of contractile elements were studied using simultaneous measurement of intracellular Ca2+ concentration ([Ca2+]i) and force of contraction in isolated canine coronary artery. Perfusion with 90 mM KCl-2.5 mM CaCl2 physiological salt solution (PSS) (90K-2.5Ca) increased [Ca2+]i and elicited a contraction. The repolarization produced by 5 mM KCl-2.5 mM CaCl2 PSS (5K-2.5Ca) or the removal of extracellular Ca2+ ([Ca2+]o) and addition of 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 90K-0Ca) induced decreases in [Ca2+]i and relaxations. The relaxation induced by 90K-0Ca was slower than that induced by 5K-2.5Ca without significant difference in the decrease in [Ca2+]i, suggesting that the Ca2+ sensitivity may be increased in depolarized muscles in 90K-0Ca. The reduction of extracellular Na+ concentration did not slow down the relaxation. The [Ca2+]i-force relation curve in 30K-0Ca was between that in 5K-0Ca and that in 90K-0Ca. The [Ca2+]i-force relationship curve obtained by changing the extracellular K+ concentration stepwise in 2.5 mM CaCl2 PSS was located to the right of that by changing [Ca2+]o in 90 mM KCl PSS. These results indicate that KCl depolarization increases the Ca2+ sensitivity of contractile elements. There may be a signal transduction system for the sarcolemma to regulate Ca2+ sensitivity of contractile elements by the level of membrane potential.