Noda M, Muramatsu I
J Cardiovasc Pharmacol. 1987 Feb;9(2):237-41. doi: 10.1097/00005344-198702000-00018.
The effects of the antianginal drug nicorandil on electrical and mechanical activity of bullfrog atria were examined. The application of nicorandil at concentrations from 0.3 to 10 mM caused a negative inotropic effect without any appreciable change in the resting membrane potential. The amplitude of action potentials was attenuated. In the voltage clamp experiments, the slow inward current was slightly inhibited, but the background inward current and delayed outward current were not affected in the presence of nicorandil. The inward rectifying properties of time-independent outward current were slightly inhibited by 10 mM nicorandil. Nicorandil inhibited the caffeine-induced contractures elicited in the depolarized preparation, but had no effect on the contracture mediated through the Na-Ca exchange mechanism. These results suggest that the negative inotropic action of nicorandil is caused by inhibition of Ca influx and intracellular mobilization of Ca. Nicorandil had little effect on the potassium conductance in this preparation.
研究了抗心绞痛药物尼可地尔对牛蛙心房电活动和机械活动的影响。应用浓度为0.3至10 mM的尼可地尔可引起负性肌力作用，而静息膜电位无明显变化。动作电位的幅度减弱。在电压钳实验中，慢内向电流略有抑制，但在尼可地尔存在下，背景内向电流和延迟外向电流不受影响。10 mM尼可地尔对非时间依赖性外向电流的内向整流特性略有抑制。尼可地尔抑制去极化制剂中咖啡因诱导的挛缩，但对通过钠钙交换机制介导的挛缩无影响。这些结果表明，尼可地尔的负性肌力作用是由抑制钙内流和细胞内钙动员引起的。尼可地尔对该制剂中的钾电导影响很小。
