健康人体中肾脏对卡托普利的反应反映了局部肾素系统的状态。

Renal response to captopril reflects state of local renin system in healthy humans.

作者信息

Fisher N D, Price D A, Litchfield W R, Williams G H, Hollenberg N K

机构信息

Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Kidney Int. 1999 Aug;56(2):635-41. doi: 10.1046/j.1523-1755.1999.00579.x.

DOI:10.1046/j.1523-1755.1999.00579.x

PMID:10432403

Abstract

BACKGROUND

Heightened activity of the renin-angiotensin system has been linked to the development of both essential hypertension and diabetic nephropathy. Blunting of the renal vasoconstrictor response to Ang II, specifically when it is corrected by angiotensin converting enzyme (ACE) inhibition, is a feature which we have employed as a marker for activation of the intrarenal RAS. In this study we tested the hypothesis that variation in the renal vasodilator response to ACE inhibition in healthy humans reflected the variation in angiotensin-mediated renal vasoconstriction provoked by a low-salt diet.

METHODS

We studied 20 healthy people (ages 19 to 57; 15 males) who were in balance on a low sodium diet. Ang II was infused for 45 minutes (3 ng/kg/min), followed by 25 mg captopril and a repeat Ang II infusion; PAH clearance was measured at the end of each interval.

RESULTS

All subjects responded to captopril with a rise in renal plasma flow (range 43 to 242, mean 118 + 12 ml/min/1.73 m2). Individual vasodilator response to captopril was a strong inverse predictor of the precaptopril vasoconstrictor response to Ang II (P = 0.006, r = -0.59). There was a stronger, positive correlation of the vasodilator response to captopril and enhancement of Ang II responsiveness after captopril (r = 0.57). Plasma renin activity was significantly correlated with captopril response among the large responders (P = 0.003; r = 0.83), but not at all among those with little response.

CONCLUSION

These results suggest substantial variation in angiotensin-mediated control of the renal circulation in healthy individuals on a low sodium intake. Variation in the vasodilator response to captopril, correlated with responses to Ang II, provides a measure of that control.

摘要

背景

肾素 - 血管紧张素系统活性增强与原发性高血压和糖尿病肾病的发生发展均有关联。肾血管对血管紧张素II（Ang II）的收缩反应减弱，特别是在通过血管紧张素转换酶（ACE）抑制得以纠正时，这一特征已被我们用作肾内肾素 - 血管紧张素系统（RAS）激活的标志物。在本研究中，我们检验了这样一个假设：健康人群中对ACE抑制的肾血管舒张反应的差异反映了低盐饮食引发的血管紧张素介导的肾血管收缩的差异。

方法

我们研究了20名健康人（年龄19至57岁；15名男性），他们处于低盐饮食平衡状态。输注Ang II 45分钟（3 ng/kg/分钟），随后给予25 mg卡托普利并重复输注Ang II；在每个时间段结束时测量对氨基马尿酸（PAH）清除率。

结果

所有受试者对卡托普利的反应均为肾血浆流量增加（范围43至242，平均118 + 12 ml/分钟/1.73 m2）。个体对卡托普利的血管舒张反应是卡托普利前对Ang II血管收缩反应的强反向预测指标（P = 0.006，r = -0.59）。卡托普利的血管舒张反应与卡托普利后Ang II反应性增强之间存在更强的正相关（r = 0.57）。在反应较大的受试者中，血浆肾素活性与卡托普利反应显著相关（P = 0.003；r = 0.83），但在反应较小的受试者中则完全不相关。