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In mesenteric artery smooth muscle cells, depolarizing voltage steps activated outward K+ currents whose amplitude was decreased by about 20% with phenylephrine (1-10 microM: n = 14 cells). Attenuation of outward current was only partly dependent on [Ca2+]i, because it persisted, although reduced, with 10 mM BAPTA in the patch pipette and was abolished in the presence of 3 mM 3,4-diaminopyridine (n = 13). In outside-out patches, phenylephrine did not exert any direct effect on the unitary current amplitude or open probability of large conductance K+ channels. Outward current was significantly increased (>100% in both cases) by 10 mM caffeine, presumably owing to the release of internal Ca2+ stores. With 10 mM BAPTA in the pipette, the only response to caffeine was a small decrease (9 +/- 3.7%, n = 10) in the K+ current. These observations show that a minor effect of phenylephrine is to reduce outward K+ current (probably Kv) in mesenteric cells.

Original publication




Journal article


Gen Pharmacol

Publication Date





389 - 399


4-Aminopyridine, Adrenergic alpha-Antagonists, Amifampridine, Animals, Caffeine, Calcium, Chelating Agents, Drug Interactions, Egtazic Acid, Female, In Vitro Techniques, Membrane Potentials, Mesenteric Arteries, Muscle Contraction, Muscle, Smooth, Vascular, Phenylephrine, Potassium, Potassium Channels, Prazosin, Rabbits, Tetraethylammonium, Vasoconstrictor Agents