Suzuki N, Gomi Y, Inagaki O, Ono K, Kasuya Y
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kanazawa University, Japan.
J Pharmacobiodyn. 1990 Mar;13(3):172-8. doi: 10.1248/bpb1978.13.172.
In the smooth muscle of the rat vas deferens, 10(-5) M cocaine shifted the dose-response curve to norepinephrine to the left and enhanced the maximal contractions to norepinephrine and methacholine. Propranolol at 10(-4) M almost completely blocked these potentiating effects of cocaine. Sotalol or lidocaine at 10(-4) M did not block the potentiating action of cocaine. The cocaine-induced enhancement of the methacholine contraction and its blockade by propranolol was observed in the dibenamine-treated vas deferens. Propranolol also blocked the depolarization-induced enhancement of the methacholine contraction. Together with the previous study demonstrating the calcium-antagonist action for propranolol, these results suggest that propranolol blocks the cocaine-induced enhancement by inhibiting the calcium influx through the potential-dependent calcium channel in the rat vas deferens.
在大鼠输精管的平滑肌中,10⁻⁵ M可卡因使去甲肾上腺素的剂量-反应曲线左移,并增强了对去甲肾上腺素和乙酰甲胆碱的最大收缩反应。10⁻⁴ M普萘洛尔几乎完全阻断了可卡因的这些增强作用。10⁻⁴ M索他洛尔或利多卡因未阻断可卡因的增强作用。在经二苄胺处理的输精管中观察到可卡因诱导的乙酰甲胆碱收缩增强及其被普萘洛尔阻断的现象。普萘洛尔还阻断了去极化诱导的乙酰甲胆碱收缩增强。结合先前证明普萘洛尔具有钙拮抗作用的研究,这些结果表明普萘洛尔通过抑制大鼠输精管中电压依赖性钙通道的钙内流来阻断可卡因诱导的增强作用。