Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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

DOI

10.1016/s0306-3623(99)00031-2

Type

Journal article

Journal

Gen Pharmacol

Publication Date

11/1999

Volume

33

Pages

389 - 399

Keywords

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