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

Abstract

Intake of nicotine has been related in many cases to acute or chronic hypertension. Using the patch–clamp technique the effect of nicotine on voltage-dependent K + channel currents in rat tail artery smooth muscle cells was studied. Nicotine at concentrations of 1–100 μM or 0.3–3 mM increased or decreased, respectively, the amplitude of the tetraethylammonium-sensitive K + currents. Pretreatment of cells with 10 μM dihydro-β-erythroidine hydrobromide, 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 μM 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 inhibitory effects of nicotine on K + channels are respectively mediated by a nicotinic receptor-dependent mechanism and by a direct interaction of nicotine with K + channels.