Further pharmacological characterization of nicotine-induced endothelium-dependent contraction in rat basilar artery

Nicotine causes an endothelium-dependent contraction in rat basilar artery and its endothelium-derived contracting factor may he leukotriene B_4 (1). The present experiments were undertaken to further characterize nicotine-induced endothelium-dependent contraction in rat basilar artery. The rat basilar artery was isolated under anesthesia (pentobarbital sodium, 50 mg/kg, i.p.) and a stainless steel needle (120 μm diameter) was inserted into the artery. The basilar artery was prepared as spiral cut preparation (about 1 mm width：about 1 cm length) by blade. Nicotine (3 × 10^-3 M)-induced endothelium-dependent contraction was not affected by the presence of L-NAME (NO synthetase inhibitor)(10^-4 M) or by the presence of arachidonic acid (10^-6 M). Combined treatment with I-NAME and arachidonic acid did not affect the contraction. Tranylcypromine (3 × 10^-4 M), which has an inhibitory action on PGI_2 synthetase, increased in the basal tone and augmented the nicotine-induced contraction. U-51605 (10^-7 -10^-5 M), which is reportedly as a PGI_2 synthetase inhibitor), increased in the basal tone and enhanced the contraction. These results suggest that in rat basilar artery, an endothelial NO and exogenous arachidonic acid may not be involved in the nicotine-induced endothelium-dependent response and PGI_2 may be involved in the response. 1 Kurahashi, K. et al. (2000) Jpn. J. Pharmacol. 82：(supple. I) 51P.