ACUTE EFFECTS OF NICOTINE ON RAT MESENTERIC VASCULATURE AND TAIL ARTERY

The effect of nicotine on adrenergic and sensory nerves was examined in tail artery ring segments and isolated perfused mesenteric vascular bed. Nicotine by itself (3 x 10(-5) and 3 x 10(-4) M) had no vasoconstrictor effect on the perfused mesentery. However, in the presence of guanethidine (5 x 10(-6) M) and methoxamine (5 x 10(-6) M), nicotine (5 x 10(-5) and 10(-4) M) caused vasodilation of 20 +/- 4 and 26 +/- 6%, respectively. The relaxation produced by nicotine was attenuated in the presence of capsaicin (3 x 10(-7) M) to desensitize sensory nerves. Higher concentrations of nicotine (3 x 10(-4) and 10(-3) M) also produced a relaxation of the mesenteric artery by 49 +/- 7 and 73 +/- 11%, respectively, an effect that was insensitive to capsaicin. The nicotinic antagonist hexamethonium (10(-5) M) blocked the relaxation produced by both low and high concentrations of nicotine. Removal of the endothelium by saponin (50 mg/ml) did not change the effect of nicotine, nor did the cyclooxygenase inhibitor indomethacin (10(-6) M). In tail artery ring segments, nicotine had no effect by itself. Nicotine (10(-5) to 10(-3) M) did not potentiate contractile responses evoked by transmural nerve stimulation, rather relaxation was produced with concentrations above 10(-4) M. These data suggest that at low concentrations nicotine activates capsaicin-sensitive sensory nerves via an action on nicotinic receptors. At higher concentrations nicotine relaxes vascular smooth muscle directly, an effect which is independent of sensory nerves. In addition, nicotine does not augment contractile responses to adrenergic nerve stimulation in the rat tail artery.