Weston A H
Department of Physiological Sciences, Medical School, University of Manchester, U.K.
J Cardiovasc Pharmacol. 1987;10 Suppl 8:S56-61.
In rat isolated portal vein, nicorandil (0.1-500 microM) abolished spontaneous tension waves and inhibited mechanical responses to norepinephrine (0.1-100 microM) and KCl (5-80 mM). Intracellular electrical recording showed that nicorandil (0.1-1 microM) abolished spontaneous multispike complexes and at higher concentrations (up to 500 microM) raised the membrane potential to approximately -90 mV. Using 86Rb as a K+-marker, nicorandil (5-500 microM) increased the 86Rb efflux rate coefficient. In rat isolated aorta, nicorandil (8-32 microM) inhibited mechanical responses to norepinephrine (0.125-100 microM) and KCl (5-80 mM), but had no effect on 86Rb exchange. In guinea pig isolated taenia caeci, nicorandil (4-64 microM) relaxed spontaneous mechanical tone and increased 86Rb efflux in the absence and presence of apamin, 100 nM. It is concluded that the inhibitory effects of nicorandil in portal vein and taenia caeci are mediated at least in part by a mechanism which involves the opening of apamin-insensitive, 86Rb-permeable K+ channels. In aorta, however, the opening of such channels was not detected, and the inhibitory effects of nicorandil in this tissue are associated with an, as yet, undefined mechanism.
在大鼠离体门静脉中，尼可地尔（0.1 - 500微摩尔）消除了自发张力波，并抑制了对去甲肾上腺素（0.1 - 100微摩尔）和氯化钾（5 - 80毫摩尔）的机械反应。细胞内电记录显示，尼可地尔（0.1 - 1微摩尔）消除了自发的多峰复合波，在较高浓度（高达500微摩尔）时将膜电位提高到约 - 90毫伏。以86Rb作为钾离子标记物，尼可地尔（5 - 500微摩尔）增加了86Rb外流速率系数。在大鼠离体主动脉中，尼可地尔（8 - 32微摩尔）抑制了对去甲肾上腺素（0.125 - 100微摩尔）和氯化钾（5 - 80毫摩尔）的机械反应，但对86Rb交换没有影响。在豚鼠离体盲肠带中，尼可地尔（4 - 64微摩尔）在有无100纳摩尔蜂毒明肽的情况下，均能松弛自发机械张力并增加86Rb外流。结论是，尼可地尔在门静脉和盲肠带中的抑制作用至少部分是由一种机制介导的，该机制涉及打开对蜂毒明肽不敏感的、可透过86Rb的钾通道。然而，在主动脉中未检测到此类通道的开放，尼可地尔在该组织中的抑制作用与一种尚未明确的机制有关。
