Huchet A M, Doursout M F, Chelly J, Schmitt H
Eur J Pharmacol. 1982 Nov 19;85(2):239-42. doi: 10.1016/0014-2999(82)90474-5.
The cardiovascular effects of AR-C 239, a new and selective alpha 1-adrenoceptor blocking drug were studied in normotensive and spontaneously hypertensive rats (SHR). AR-C 239 (300 micrograms/kg i.v.) did not change the heart rate in control (without pretreatment) and bilaterally vagotomized normotensive rats, but induced significant bradycardia in rats pretreated with a beta-adrenoceptor blocking drug. This bradycardic effect was inhibited by atropine or bilateral vagotomy. In SHR, the administration of AR-C 239 reduced heart rate in the control, bilaterally vagotomized and beta-blocked rats. Blood pressure was decreased in the same way in the two rat strains. It is suggested that central alpha 1-adrenoceptors could participate in the control of vagal tone in normotensive and SH rats, and of sympathetic activity in the SHR only.
研究了新型选择性α1肾上腺素受体阻断药AR-C 239对正常血压大鼠和自发性高血压大鼠(SHR)的心血管作用。AR-C 239(静脉注射300微克/千克)在对照(未预处理)和双侧迷走神经切断的正常血压大鼠中未改变心率,但在用β肾上腺素受体阻断药预处理的大鼠中诱导出显著的心动过缓。这种心动过缓效应被阿托品或双侧迷走神经切断所抑制。在SHR中,给予AR-C 239可降低对照、双侧迷走神经切断和β受体阻断大鼠的心率。两种大鼠品系的血压均以相同方式降低。提示中枢α1肾上腺素受体可能仅参与正常血压大鼠和SH大鼠迷走神经张力的控制,以及仅在SHR中参与交感神经活动的控制。