Delles Christian, Klingbeil Arnfried U, Schneider Markus P, Handrock Renate, Weidinger Gottfried, Schmieder Roland E
Department of Medicine IV/4, University of Erlangen-Nürnberg, Nuremberg, Germany.
Am J Hypertens. 2003 Dec;16(12):1030-5. doi: 10.1016/j.amjhyper.2003.07.017.
To elucidate the renoprotective mechanism of AT(1)-receptor blockers, we compared the effects of the AT(1)-receptor blocker valsartan with those of the calcium channel blocker amlodipine on renal hemodynamics and microcirculation.
A total of 58 patients (50.2 +/- 9.0 years) with mild to moderate essential hypertension were included in a randomized, double-blind study to receive either valsartan (80 to 160 mg) or amlodipine (5 to 10 mg). Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured before and after 8 weeks of treatment. Glomerular hydrostatic pressure (P(Glo)) and resistances of the afferent (R(A)) and efferent (R(E)) arterioles were calculated according to the Gomez formulas.
Blood pressure control was similar in both groups. RPF did not change with either treatment. In contrast, GFR increased with amlodipine (+8 +/- 14 mL/min; P <.01) but was preserved with valsartan. Amlodipine caused a more marked increase in the R(E)/R(A) ratio than valsartan (+0.26 +/- 0.26 v +0.13 +/- 0.24, P <.05), which was paralleled by an increase in P(Glo) in patients treated with amlodipine (+1.9 +/- 4.3 mm Hg; P <.05) but not in those treated with valsartan.
At similar blood pressure control, valsartan maintained GFR and P(Glo), whereas amlodipine led to glomerular hyperfiltration and an increase in P(Glo). The results might explain the favorable renal outcome with AT(1)-receptor blocker therapy.
为阐明血管紧张素Ⅱ1型（AT(1)）受体阻滞剂的肾脏保护机制，我们比较了AT(1)受体阻滞剂缬沙坦与钙通道阻滞剂氨氯地平对肾脏血流动力学和微循环的影响。
58例（年龄50.2±9.0岁）轻度至中度原发性高血压患者纳入一项随机双盲研究，接受缬沙坦（80至160mg）或氨氯地平（5至10mg）治疗。在治疗8周前后测量肾血浆流量（RPF）和肾小球滤过率（GFR）。根据戈麦斯公式计算肾小球静水压（P(Glo)）以及入球小动脉（R(A)）和出球小动脉（R(E)）的阻力。
两组血压控制情况相似。两种治疗方法均未使RPF发生改变。相比之下，氨氯地平使GFR升高（+8±14ml/分钟；P<.01），而缬沙坦则维持GFR不变。氨氯地平使R(E)/R(A)比值升高幅度大于缬沙坦（+0.26±0.26对+0.13±0.24，P<.05），与之相应，接受氨氯地平治疗的患者P(Glo)升高（+1.9±4.3mmHg；P<.05），而接受缬沙坦治疗的患者则未升高。
在血压控制相似的情况下，缬沙坦维持GFR和P(Glo)，而氨氯地平导致肾小球高滤过和P(Glo)升高。这些结果可能解释了AT(1)受体阻滞剂治疗具有良好肾脏结局的原因。
