Arnerić S P, Long J P
J Pharm Pharmacol. 1984 May;36(5):318-21. doi: 10.1111/j.2042-7158.1984.tb04382.x.
The cardiovascular effects of RDS-127 [2-di-n-propylamino-4,7-dimethoxyindane] were examined in normotensive, anaesthetized rats. RDS-127 given i.v. (12.5-125 micrograms kg-1) produced dose-dependent bradycardia. The bradycardic effect was 20.5 times more potent when the drug was administered intracerebroventricularly (i.c.v.) than when given i.v. RDS-127 produced a slight, but significant hypotension. Haloperidol given i.c.v. or i.v. reversed these bradycardic and hypotensive actions, whereas phentolamine was ineffective. Methylatropine partially reduced the bradycardic effect. These results suggest that RDS-127 activates central DA receptors to produce hypotension and bradycardia in rats.
在正常血压的麻醉大鼠中研究了RDS-127[2-二正丙基氨基-4,7-二甲氧基茚满]的心血管效应。静脉注射(12.5-125微克/千克)RDS-127可产生剂量依赖性心动过缓。当药物脑室内注射(i.c.v.)时,心动过缓效应比静脉注射时强20.5倍。RDS-127产生轻微但显著的低血压。脑室内或静脉注射氟哌啶醇可逆转这些心动过缓和低血压作用,而酚妥拉明无效。甲基阿托品部分降低了心动过缓效应。这些结果表明,RDS-127激活中枢多巴胺受体,在大鼠中产生低血压和心动过缓。