The role of calcium channel in the effect of nicotine on contractility in isolated toad ventricle

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Abstract
The mechanism of the positive inotropic effect produced by nicotine (6.2 × 10−5 mol/l to 4.9 × 10−4 mol/l) on electrically driven toad ventricles was investigated. The response to nicotine was not affected by 6-hydroxydopamine pretreament, bretylium (2.4 × 10−4 mol/l) exposure or tyramine tachyphylaxis. Following desensitisation by isoprenaline (4.2 × 10−6 mol/l) of the beta-adrenoceptor in the ventricles, the response to nicotine was no affected. However, the response was antagonised by ethylene diamine tetraethyl acetate (2.3 × 10−4 mol/l), verapamil (0.4 × 10−5 mol/l) or calcium-free Ringer. Nicotine prolonged the action potential duration and enhanced the force of contraction. Nicotine induced slow action potentials in partially depolarized (in high potassium solution) ventricles and this was antagonised by verapamil (0.4 × 10−5 mol/l). These results suggest that the effects of nicotine are mediated by a direct interaction with the Ca2+ channels at the cell surface.