NICOTINE AND POTASSIUM CHLORIDE CONTRACTURE IN MAMMALIAN VENTRICLE

¹ Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York

The action of nicotine on contracture force in depolarized mammalian ventricle was evaluated. Papillary and trabecular muscles dissected from the right ventricle of cats were maintained at 27-30°C and stimulated at 6 to 30 beats/min under isometric recording conditions. Contractures were induced by replacing NaCl with 100 to 140 mM KCl in the Tyrode's medium. Flow rate during contracture was held constant at either 14 ml/min (low flow) or 140 ml/min (high flow). Propranolol (1 x 10^-6 M) had little effect on maximal potassium-induced contracture force. Nicotine (0.03-12.4 mM) did not induce contracture in normal or beta receptor blocked muscle maintained in control Tyrode's solution containing 4.0 mM potassium. Nicotine (6.2 and 12.4 mM) increased contracture force in potassium-depolarized muscle in the presence and absence of calcium at low flow and in the absence of calcium at high flow; the same concentrations had little effect on high-potassium contractures in the presence of calcium at high flow. Nicotine may influence contracture force in depolarized cat ventricular muscle by releasing sarcolemmal stores of calcium. This action may be affected by formation of nicotine-calcium complexes and the flow rate utilized during high-potassium contracture.