The membrane potential and tension were recorded during contracture of mammalian ventricular muscles bathed in Tyrode solution with Ba2+ in the place of Ca2+. Strength of contracture increased with increasing Ba2+ concentration from 0.1 to 4 mM and reached a plateau above 4 mM. The membrane potential was depolarized to about -35 mV with 0.1 mM Ba2+ and to -20 mV with 5 mM Ba2+. When 0.5 mM Mn2+ was added to Ba2+-Tyrode solution, in which the muscle had been in a state of steady contracture, the muscle immediately started to relax to the resting level. In contrast, addition of 2 micrograms/ml epinephrine to Ba2+-Tyrode solution increased the strength of the contracture. Neither epinephrine nor Mn2+ caused any noticeable changes of the depolarized membrane potential. The results suggest that Ba2+ not only activates the contractile system but also depolarizes the membrane potential independently of activating the contractile system. These two remarkable actions of Ba2+ seem to be responsible for the long-lasting contracture.
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