Phillips C A, Mylecharane E J, Markus J K, Shaw J
Eur J Pharmacol. 1985 May 20;111(3):319-27. doi: 10.1016/0014-2999(85)90638-7.
The intravenous (i.v.) administration of ketanserin (0.1-0.4 mg/kg) produced immediate and sustained decreases in systemic blood pressure and heart rate in pentobarbitone-anaesthetized dogs. These doses of ketanserin did not inhibit common carotid vasoconstrictor responses to intraarterial (i.a.) noradrenaline, pre-ganglionic stimulation of the sectioned cervical sympathetic nerve, or i.v. nicotine, thus the effects of ketanserin are not due to blockade of vascular alpha-adrenoceptors, adrenergic neurone blockade, or ganglionic blockade. Systemic pressor responses to i.v. nicotine, which produces sympathetic activation by both central and ganglionic stimulating actions, and to common carotid artery occlusion, were inhibited by 0.1-0.4 mg/kg of ketanserin i.v. These results suggest that in the anaesthetized dog, the hypotensive action of ketanserin involves a centrally mediated inhibition of sympathetic tone. Peripheral vascular 5-HT2 receptor blockade does not appear to be responsible for the hypotensive effect of ketanserin in this model, although this does not preclude the involvement of such a mechanism in its clinical antihypertensive action.
在戊巴比妥麻醉的犬中，静脉注射酮色林（0.1 - 0.4毫克/千克）可使全身血压和心率立即且持续下降。这些剂量的酮色林并不抑制颈总动脉对动脉内注射去甲肾上腺素、切断的颈交感神经节前刺激或静脉注射尼古丁的血管收缩反应，因此酮色林的作用并非由于阻断血管α - 肾上腺素能受体、肾上腺素能神经元阻滞或神经节阻滞。静脉注射尼古丁（通过中枢和神经节刺激作用产生交感神经激活）以及颈总动脉闭塞引起的全身升压反应，可被静脉注射0.1 - 0.4毫克/千克的酮色林所抑制。这些结果表明，在麻醉犬中，酮色林的降压作用涉及中枢介导的交感神经张力抑制。在该模型中，外周血管5 - HT2受体阻断似乎并非酮色林降压作用的原因，尽管这并不排除这种机制参与其临床抗高血压作用。
