Lyons D, Webster J, Benjamin N
Department of Medicine and Therapeutics, University of Aberdeen, UK.
Eur J Clin Pharmacol. 1994;47(2):147-50. doi: 10.1007/BF00194964.
It has been proposed that the suppression of endogenous levels of angiotensin II by angiotensin converting enzyme inhibition, may result in up-regulation of vascular AT1 receptors. This study evaluated the effects of orally administered enalapril on angiotensin II induced vasoconstriction in the human forearm of patients with mild-moderate hypertension. Patients received in random order, enalapril (20 mg) or matched placebo daily for 2 weeks. Forearm blood flow response to increasing doses of angiotensin II was measured using venous occlusion plethysmography at the beginning of the study and at the end of each 2 week treatment period. Treatment with enalapril significantly reduced plasma angiotensin II levels and supine blood pressure compared to placebo. The percentage reductions in forearm blood flow in the infused arm, in response to the maximum dose of angiotensin II (50 pmol.min-1) were 53.2% at baseline, 51.4% on placebo and 59.5% on enalapril. The differences were not significantly different. This study demonstrates that suppression of plasma angiotensin II does not enhance the response to exogenous intra-arterial angiotensin II in the human forearm of mild-moderately hypertensive patients.
有人提出,通过抑制血管紧张素转换酶来降低内源性血管紧张素II水平,可能会导致血管AT1受体上调。本研究评估了口服依那普利对轻中度高血压患者人前臂中血管紧张素II诱导的血管收缩的影响。患者按随机顺序,每日服用依那普利(20毫克)或匹配的安慰剂,共2周。在研究开始时以及每个2周治疗期结束时,使用静脉阻塞体积描记法测量前臂血流对递增剂量血管紧张素II的反应。与安慰剂相比,依那普利治疗显著降低了血浆血管紧张素II水平和仰卧位血压。在输注臂中,对最大剂量血管紧张素II(50皮摩尔·分钟-1)反应时,前臂血流减少的百分比在基线时为53.2%,安慰剂组为51.4%,依那普利组为59.5%。差异无统计学意义。本研究表明,在轻中度高血压患者的人前臂中,抑制血浆血管紧张素II并不会增强对外源性动脉内血管紧张素II的反应。