The action potential duration (APD) of histamine-induced slow action potentials (SAP) and force of contraction (FC) were potentiated by nicotine (0.6-1.0 mmol.L-1) on guinea pig papillary muscles in a concentration-dependent manner. In the presence of atropine, nicotine concentration dependently suppressed the action potential amplitude (APA), APD, the maximal upstroke velocity (Vmax), and FC in catecholamine-depleted (reserpine 2.5 mg.kg-1 ip, 15 h prior to the experiment) muscles. Nicotine (0.6 mmol.L-1) itself induced SAP and enhanced FC. These 2 effects were antagonized by verapamil. A linear relationship existed between APA of nicotine-induced SAP and 1g [Ca2+]0 with a slope of 23.2 mV for a 10-fold change in [Ca2+]0. These results suggested that the effects of nicotine on enhancing Isi were mediated by the release of catecholamines in myocardium.