Koley J, Saha J K, Koley B
Naunyn Schmiedebergs Arch Pharmacol. 1987 Jan;335(1):86-90. doi: 10.1007/BF00165041.
The mechanism of the positive inotropic effect produced by nicotine (6.2 X 10(-5) mol/l to 4.9 X 10(-4) mol/l) on electrically driven toad ventricles was investigated. The response to nicotine was not affected by 6-hydroxydopamine pretreatment, bretylium (2.4 X 10(-4) mol/l) exposure or tyramine tachyphylaxis. Following desensitisation by isoprenaline (4.2 X 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 X 10(-4) mol/l), verapamil (0.4 X 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 X 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.
研究了尼古丁（6.2×10⁻⁵摩尔/升至4.9×10⁻⁴摩尔/升）对电驱动蟾蜍心室产生正性肌力作用的机制。对尼古丁的反应不受6-羟基多巴胺预处理、溴苄铵（2.4×10⁻⁴摩尔/升）暴露或酪胺快速耐受的影响。在用异丙肾上腺素（4.2×10⁻⁶摩尔/升）使心室中的β-肾上腺素能受体脱敏后，对尼古丁的反应不受影响。然而，该反应被乙二胺四乙酸（2.3×10⁻⁴摩尔/升）、维拉帕米（0.4×10⁻⁵摩尔/升）或无钙林格液拮抗。尼古丁延长动作电位持续时间并增强收缩力。尼古丁在部分去极化（在高钾溶液中）的心室中诱导慢动作电位，这被维拉帕米（0.4×10⁻⁵摩尔/升）拮抗。这些结果表明，尼古丁的作用是通过与细胞表面的Ca²⁺通道直接相互作用介导的。
