Abstract
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.
Published Version
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