Nicotine-induced NO-mediated increase in cortical cerebral blood flow is blocked by β2-adrenoceptor antagonists in the anesthetized rats

Involvement of nitric oxide (NO) and β-adrenoceptors in an increase in the cortical cerebral blood flow (CBF) following an intravenous (i.v.) injection of a small dose of nicotine which did not affect the systemic blood pressure in the rats was investigated. I.v. injection of nicotine (30 μg/kg) for 1 min produced a significant increase in CBF lasting for more than 20 min without a significant effect on the systemic blood pressure. I.v. injection of L -NG-nitroarginine methylester (30 mg/kg) significantly attenuated nicotine-induced increase in the cortical CBF. The attenuation was reversed by i.v. injection of L -arginine (300 mg/kg), suggesting an intimate role of nitric oxide (NO) in nicotine-induced increase in the cortical CBF. The nicotine-induced increase in the cortical CBF was significantly attenuated by propranolol (10 mg/kg, i.v.) and ICI 118, 551 (a β2-adrenoceptor antagonist, 10 mg/kg, i.v.) but not by metoprolol (a β1-adrenoceptor antagonist, 10 mg/kg, i.v.). β2-adrenoceptors on presynaptic nitrergic nerves may be involved in nicotine-induced NO-mediated increase in the cortical CBF.