Abstract
Nicotine, 0.01–0.1 mm, evoked a positive inotropic response and abolished the "staircase" and poststimulation potentiation in toad ventricular muscle; 0.2 mm nicotine caused the development of contracture, whether or not extracellular Ca++ was present; and 1.0 mm nicotine enhanced the uptake and release of Ca45 from the muscle. It seems probable that the effect of nicotine on the contractile response of cardiac muscle can be related to the mobilization of Ca++.