Modification of the Inotropic Activity of Calcium by Potassium

Abstract

IN previous communications from this laboratory^1,2, results have been presented which suggest that the accumulation of calcium at specific sites on or about the membranes defining individual cardiac cells may provide the fundamental basis for the conditions of enhanced contractility recorded during post- and extra-systolic potentiation and throughout the classical staircase³. These results confirmed the earlier observations of Niedergerke⁴ and support the hypotheses of Sandow⁵, of Csapo⁶, and of Bianchi and Shanes⁷, who maintain that entry of calcium associated with the depolarization stage of activation is involved both in the link between excitation and contraction and in the regulation of the contractile force. Hajdu and Szent-Györgyi⁸, however, having observed that the staircase in isolated perfused frog hearts was abolished by reducing the potassium concentration, [K⁺], of the perfusate suggested that progressive loss of potassium from the myocardium during successive beats of the staircase provided the basis for the increased contractility.