Effects of nicotine on K+ channel currents in vascular smooth muscle cellsfrom rat tail arteries

Intake of nicotine has been related in many cases to acute or chronic hyper tension. Using the patch-clamp technique the effect of nicotine on voltage- dependent K+ channel currents in rat tail artery smooth muscle cells was st udied. Nicotine at concentrations of 1-100 mu M or 0.3-3 mM increased or de creased, respectively, the amplitude of the tetraethylammonium-sensitive K currents. Pretreatment of cells with 10 mu M dihydro-beta-erythroidine hyd robromide, a nicotinic receptor antagonist, abolished the excitatory effect (n = 6), but not the inhibitory effect (n = 10), of nicotine on K+ channel currents. The activation of nicotinic receptors with 100 mu M 1,1-dimethyl -4-phenylpiperazinium iodide increased K+ channel currents by 27.4 +/- 3.8% (n = 13, P < 0.01). Our results indicate that the excitatory and inhibitor y effects of nicotine on K+ channels are respectively mediated by a nicotin ic receptor-dependent mechanism and by a direct interaction of nicotine wit h K+ channels. (C) 1999 Elsevier Science B.V. All rights reserved.