Schmieder R E, Schobel H P, Gatzka C E, Häuser W, Dominiak P, Mann J F, Luft F C
Department of Medicine IV-Nephrology, University of Erlangen-Nürnberg, Germany.
J Hypertens. 1996 Oct;14(10):1201-7. doi: 10.1097/00004872-199610000-00008.
To examine the effects of angiotensin converting enzyme (ACE) inhibition on renal and systemic haemodynamics as well as on humoral regulators, under resting conditions and during mental stress in 20 normotensive and 20 mildly hypertensive subjects.
All of the subjects received either 25 mg cilazapril or placebo once a day, in a randomized, double-blind, cross-over trial for 1 week, followed by a 2-week washout period before the alternative regimen was given. We measured renal blood flow with para-aminohippuran, glomerular filtration rate with inulin, cardiac output by impedance cardiography and blood pressure and heart rate by an oscillometric method. We also monitored effects on plasma renin activity, aldosterone, catecholamines and atrial natriuretic peptide. Mental stress consisted of a long-lasting, time-reaction device, thereby provoking activation of the sympathetic nervous system.
At rest ACE inhibition lowered mean arterial pressure (92 +/- 10 versus 98 +/- 9 mmHg), increased renal blood flow (803 +/- 109 versus 707 +/- 93 ml/min) and the renal fraction of cardiac output (25.9 +/- 2.5 versus 23.5 +/- 2.5%) and decreased the filtration fraction (17.9 +/- 2.5 versus 19.8 +/- 2.7%) in hypertensive but not in normotensive subjects. Sympathetic activation by mental stress leading to a transient increase in blood pressure did not alter significantly the effects of ACE inhibition on renal and systemic haemodynamics, in normotensive or in hypertensive subjects, although a tendency towards attenuation of the rise in glomerular filtration rate was noted in hypertensives (7.2 +/- 1.0 versus 5.1 +/- 0.8%). ACE inhibition led to increased plasma noradrenaline at rest but not during mental stress in hypertensive patients.
ACE inhibition in patients with mild hypertension increased selectively renal perfusion, which is conserved during mental stress without persistent effects on the sympathetic nervous system. Thus, mental stress as a correlate of daily life stress appeared not to confound the selective renal vasodilatory effect of ACE inhibitors.
研究血管紧张素转换酶(ACE)抑制剂对20名血压正常者和20名轻度高血压患者在静息状态及精神应激时肾脏和全身血流动力学以及体液调节因子的影响。
在一项随机、双盲、交叉试验中,所有受试者每天服用一次25毫克西拉普利或安慰剂,为期1周,随后有2周的洗脱期,之后给予另一种治疗方案。我们用对氨基马尿酸测量肾血流量,用菊粉测量肾小球滤过率,用阻抗心动图测量心输出量,用示波法测量血压和心率。我们还监测了对血浆肾素活性、醛固酮、儿茶酚胺和心房利钠肽的影响。精神应激由一个持续时间长的时间反应装置诱发,从而激活交感神经系统。
静息时,ACE抑制剂降低了高血压患者的平均动脉压(92±10对98±9 mmHg),增加了肾血流量(803±109对707±93 ml/min)和心输出量的肾部分(25.9±2.5对23.5±2.5%),并降低了滤过分数(17.9±2.5对19.8±2.7%),而血压正常者无此变化。精神应激导致血压短暂升高,交感神经激活,但在血压正常或高血压患者中,ACE抑制剂对肾脏和全身血流动力学的影响未发生显著改变,不过高血压患者肾小球滤过率升高的幅度有减弱趋势(7.2±1.0对5.1±0.8%)。ACE抑制剂使高血压患者静息时血浆去甲肾上腺素增加,但精神应激时未增加。
轻度高血压患者使用ACE抑制剂可选择性增加肾脏灌注,在精神应激时这种作用得以保留,且对交感神经系统无持续影响。因此,作为日常生活应激相关因素的精神应激似乎并未混淆ACE抑制剂的选择性肾血管舒张作用。