High K+,Na+-deficient solution inhibits tension, O2 consumption, and ATP synthesis in smooth muscle.

In guinea pig taenia coli, added 45.4 mM K+ induced a sustained contraction, increased the rate of oxygen consumption, and slightly decreased the ATP content. In substituted 154.2 mM K+, Na+-deficient solution, only a transient contraction was induced. Oxygen consumption also showed only a transient increase and ATP content of the muscle rapidly decreased. Such an inhibition of sustained contraction and the decrease in both oxygen consumption and ATP content were recovered when 5.5 mM pyruvate or 50 mM NaCl was added during the 154.2 mM K+-induced contraction. In rabbit aorta, substituted 80 mM K+, 74.2 mM Na+ solution induced a sustained contraction, increase in oxygen consumption, and no change in ATP content. The 80 mM K+ solution without added glucose also induced a sustained contraction followed by a slight increase in oxygen consumption and a slight decrease in ATP content. The 154.2 mM K+, Na+-deficient solution produced similar changes in both oxygen consumption and ATP content as the 80 mM K+, glucose depleted solution. However, the 154.2 mM K+ solution induced only a transient contraction in the vascular smooth muscle. When 100 mM sucrose was hyperosmotically added to the 154.2 mM K+ solution, the suppressed muscle tension increased again, although the ATP content did not increase. From these and the previous results, it is concluded that glucose utilization by the taenia coli is inhibited in the 154.2 mM K+, Na+-deficient solution, and the decreased energy production of the muscle cell does not compensate the increased energy consumption induced by the high concentration of K+. In the aorta, although the Na+-deficient solution also decreases ATP production, it is the cell swelling induced by a high KCI concentration in the medium, not the decrease in energy metabolism, that has a direct inhibitory effect on muscle tension.