Potentiation of contraction in bullfrog ventricle strips by manganese and nickel.

Sodium-lack contractures by strips of bullfrog ventricle were found to be increased in the presence of manganous ion (1-10 mM). In addition, peak force development was usually attained earlier in the presence of manganous ion and the rate of relaxation was decreased by nickel (0.7-2.0 mM), although the latter cation did not potentiate contractural force. Both manganese and nickel had only depressant effects on potassium-excess contractures, as well as on electrically stimulated twitches. Depressant effects of manganese and nickel on sodium-lack contractures were also found. These were smaller, the lower the extracellular sodium concentration and the higher the extracellular calcium concentration. When these well-known negative inotropic effects of the divalent cations were suppressed in sodium-free, calcium-rich media, their potentiating effects were unmasked, resulting in marked augmentation by these cations of potassium-excess contractures and of twitches, along with slowing of relaxation. Experimental maneuvers that have been reported to bring about entry of manganese into these cardiac cells did not increase the observed positive inotropic effect. It thus seems probable that these ions act on the membrane of the ventricle fiber. Also, in view of earlier evidence that they neither affect myofibrillar function nor induce calcium release from mitochondria, it is provisionally concluded that the mechanism of their potentiating effect on mechanical activation is due to their inhibition of calcium extrusion from the fibers, described in the accompanying paper.