Bell C
Br J Pharmacol. 1982 Jun;76(2):231-3. doi: 10.1111/j.1476-5381.1982.tb09211.x.
After blockade of noradrenergic transmission with guanethidine in anaesthetized dogs, stimulation of the peripheral end of the cut tibial nerve (1 Hz, 10 pulses) produces a vasodilator response which is localized to the circulation of the paw pads. The time course of the response is considerably prolonged after systemic administration of the dopamine-uptake blocking drug, benztropine (1 mg/kg). This effect is not due to inhibition of Uptake 1, as benztropine, unlike desmethylimipramine, does not prolong responses to noradrenergic vasoconstrictor nerve stimulation. The results support previous evidence suggesting that the dilator response to tibial nerve stimulation involves neural release of dopamine.
在对麻醉犬用胍乙啶阻断去甲肾上腺素能传递后,刺激切断的胫神经外周端(1赫兹,10个脉冲)会产生一种血管舒张反应,该反应局限于爪垫的循环系统。在全身给予多巴胺摄取阻断药物苯海索(1毫克/千克)后,该反应的时间进程显著延长。这种效应并非由于对摄取1的抑制,因为与去甲丙咪嗪不同,苯海索不会延长对去甲肾上腺素能血管收缩神经刺激的反应。这些结果支持了先前的证据,表明对胫神经刺激的舒张反应涉及多巴胺的神经释放。