Ramírez A J, Enero M A
Acta Physiol Lat Am. 1980;30(3):199-203.
The mechanisms involved in the hypotensive effect of apomorphine were studied in urethane anesthetized rats. The intravenous injection of apomorphine (0.01-0.75 mg/kg) produced a dose dependent fall in mean blood pressure. At the higher doses used (0.5-0.75 mg/kg) a marked bradycardia accompanied the hypotensive effect. These cardiovascular effects were prevented by pretreating the animals with pimozide (0.01-0.1 mg/kg). Low doses of haloperidol (0.03-0.3 mg/kg) did not antagonize the hypotensive action of apomorphine. Higher doses of haloperidol (1-3 mg/kg) reduced markedly the mean blood pressure. Atropine (1 mg/kg) partially antagonized the decrease in mean blood pressure induced by apomorphine and prevented completely the bradycardia. Hexamethonium (10 mg/kg) reduced the mean blood pressure and when apomorphine was administered, a residual hypotensive effect and no bradycardia was observed. It is concluded that the cardiovascular actions of apomorphine are central in origin and mainly due to the stimulation of a dopamine receptor. A probable peripheral effect could not be discarded.
在乌拉坦麻醉的大鼠中研究了阿扑吗啡降压作用的机制。静脉注射阿扑吗啡(0.01 - 0.75毫克/千克)可使平均血压呈剂量依赖性下降。在使用较高剂量(0.5 - 0.75毫克/千克)时,降压作用伴有明显的心动过缓。用匹莫齐特(0.01 - 0.1毫克/千克)预处理动物可防止这些心血管效应。低剂量的氟哌啶醇(0.03 - 0.3毫克/千克)不能拮抗阿扑吗啡的降压作用。较高剂量的氟哌啶醇(1 - 3毫克/千克)可显著降低平均血压。阿托品(1毫克/千克)部分拮抗阿扑吗啡引起的平均血压下降,并完全防止心动过缓。六甲铵(10毫克/千克)降低平均血压,当给予阿扑吗啡时,观察到残留的降压作用且无心动过缓。结论是,阿扑吗啡的心血管作用起源于中枢,主要是由于多巴胺受体的刺激。不能排除可能的外周效应。