Tomlinson B, Renondin J C, Graham B R, Prichard B N
Department of Clinical Pharmacology, University College and Middlesex School of Medicine, London.
Eur J Clin Pharmacol. 1991;41(1):1-3. doi: 10.1007/BF00280097.
Intravenous urapidil, 40 mg bolus followed by an infusion of 18 mg.h-1 for 2 h was administered to 6 female non-patient volunteers. Randomised cumulative dose response curves to angiotensin, phenylephrine and isoprenaline were performed before and commencing 30 min after the start of the infusion of urapidil. Urapidil significantly reduced supine systolic blood pressure, 118.5 mm Hg to 105.3. The diastolic blood pressure was not significantly reduced, heart rate was not affected. Urapidil did not affect the responses to angiotensin or isoprenaline. Urapidil inhibited the pressor response to phenylephrine. The dose required to increase systolic blood pressure by 20 mm Hg increased from 156.9 micrograms.min-1 before to 685 micrograms.min-1 during urapidil; Dose ratio from individual values of 4.58. Urapidil concentrations were not significantly different before and after each agonist infusion. It is concluded that urapidil has alpha 1-adrenoceptor blocking activity in man without any non specific vasodilator action and that it is devoid of beta adrenoceptor blocking action.
对6名女性非患者志愿者静脉注射40毫克乌拉地尔推注剂量,随后以18毫克/小时的速度输注2小时。在输注乌拉地尔开始前及开始后30分钟,分别绘制对血管紧张素、去氧肾上腺素和异丙肾上腺素的随机累积剂量反应曲线。乌拉地尔显著降低仰卧位收缩压,从118.5毫米汞柱降至105.3毫米汞柱。舒张压未显著降低,心率未受影响。乌拉地尔不影响对血管紧张素或异丙肾上腺素的反应。乌拉地尔抑制对去氧肾上腺素的升压反应。使收缩压升高20毫米汞柱所需的剂量,从乌拉地尔给药前的156.9微克/分钟增加至给药期间的685微克/分钟;个体值的剂量比为4.58。每次激动剂输注前后乌拉地尔浓度无显著差异。结论是,乌拉地尔在人体具有α1肾上腺素能受体阻断活性,无任何非特异性血管舒张作用,且无β肾上腺素能受体阻断作用。