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Abstract
This study shows that cromakalim (0.4–10 μM) can concentration-dependently hyperpolarize the smooth muscle cell membrane and increase 86Rb efflux from rabbit mesenteric small arteries at concentrations which inhibit noradrenaline-induced increases in perfusion pressure in this preparation. Hyperpolarisation of the cell membrane by cromakalim was inhibited by prior exposure of the tissue to glibenclamide (1 μM). Noradrenaline (> 1 μM) depolarized the smooth muscle cell membrane and this effect was reduced in the presence of cromakalim. Experiments involving repetitive stimulation of the perivascular nerves in this tissue showed that cromakalim (2–10 μM) reduced excitatory junction potential amplitude and fall time without affecting the facilitation process. The results of this study suggest that in rabbit small mesenteric arteries the vasodilator action of cromakalim is a consequence of the opening of 86Rb-permeable potassium channels. It is unlikely that any component of the vasorelaxant effects of cromakalim is due to a direct effect on voltage-operated calcium channels or a prejunctional effect on neuroeffector transmission.
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