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.
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