Suemaru K, Gomita Y, Furuno K, Araki Y
Department of Hospital Pharmacy, Okayama University Medical School, Japan.
Pharmacol Biochem Behav. 1993 Sep;46(1):131-3. doi: 10.1016/0091-3057(93)90328-q.
The effects of various beta-adrenergic receptor antagonists on nicotine-induced tail-tremor were investigated in rats. Atenolol (5 and 10 mg/kg, IP), arotinolol (5 and 10 mg/kg, IP), and carteolol (5 and 10 mg/kg, IP), hydrophilic beta-adrenergic receptor antagonists, did not affect the tail-tremor induced by nicotine given at a dose of 0.5 mg/kg SC. However, propranolol (5-20 mg/kg, IP) and pindolol (5-20 mg/kg, IP), nonselective and lipophilic beta-adrenergic receptor antagonists, did suppress the tail-tremor dose dependently. In contrast, metoprolol (5-20 mg/kg, IP), lipophilic and beta 1-selective adrenergic receptor antagonists, did not show such an effect. These results suggest that nicotine-induced tail-tremors may be mediated through central beta 2-adrenergic receptors as an appearance and developmental mechanism.
研究了各种β-肾上腺素能受体拮抗剂对大鼠尼古丁诱导的尾部震颤的影响。阿替洛尔(5和10mg/kg,腹腔注射)、阿罗洛尔(5和10mg/kg,腹腔注射)和卡替洛尔(5和10mg/kg,腹腔注射),亲水性β-肾上腺素能受体拮抗剂,不影响皮下注射0.5mg/kg尼古丁诱导的尾部震颤。然而,普萘洛尔(5-20mg/kg,腹腔注射)和吲哚洛尔(5-20mg/kg,腹腔注射),非选择性和亲脂性β-肾上腺素能受体拮抗剂,确实剂量依赖性地抑制了尾部震颤。相比之下,美托洛尔(5-20mg/kg,腹腔注射),亲脂性和β1选择性肾上腺素能受体拮抗剂,没有显示出这样的效果。这些结果表明,尼古丁诱导的尾部震颤可能通过中枢β2-肾上腺素能受体作为一种表现和发展机制介导。