Hu L, Catanzaro D F, Pitarresi T M, Laragh J H, Sealey J E
Cardiovascular Center, New York Hospital-Cornell University Medical College, New York 10021, USA.
J Hypertens. 1998 Sep;16(9):1285-98. doi: 10.1097/00004872-199816090-00010.
To investigate whether plasma angiotensin II (Ang II) determines the effects of the renin-angiotensin system or whether tissue uptake of renin and localized production of Ang II might account for any cardiovascular, renal, hormonal or drinking effect of circulating renin.
Intravenous infusions of renin (0.6 ng/min; n = 10) and Ang II (3.5 ng/min; n = 10) that produce similar plasma Ang II levels were compared for 2 weeks with vehicle (n = 7) in conscious rats after a 1-week control period. Mean arterial pressure (MAP) and the heart rate were measured continuously. Hormones and renal function were measured twice weekly. Plasma Ang II and recovery data were measured in seven additional rats.
In renin- and Ang II-infused rats, respectively, plasma Ang II increased similarly from 4.5 +/- 0.8 and 4.4 +/- 0.9 to 10.8 +/- 0.7 and 10.6 +/- 0.7 pg/ml and declined similarly in the second week to 7.0 +/- 1.1 and 7.0 +/- 1.5 pg/ml. Plasma renin increased from 4.2 +/- 0.7 to 21.7 +/- 1.3 and fell from 5.9 +/- 0.5 to 0.6 +/- 0.2 ng/ml per h respectively. Plasma prorenin fell similarly (> 70%); angiotensinogen was unchanged. MAP rose initially by 25.6 +/- 1.2 and 23.3 +/- 0.9 mmHg and by an additional 21.1 +/- 2.4 and 27.4 +/- 1.8 mmHg on days 5-8. The heart rate fell gradually but transiently by -11% in both. Although the initial MAP rise was slower in renin-infused rats (P< 0.05) MAP returned to baseline within 2 h after both infusions were stopped. Changes in renal vascular resistance, renal blood flow, glomerular filtration rate, urinary sodium, potassium and water excretion and water intake were not significantly different between renin- and Ang II-infused rats.
Intravenous infusions of low doses of renin or Ang II into conscious rats increase MAP identically. MAP increases in two phases 5-8 days apart, in coordination with transient falls in the heart rate. Renin- and Ang II-induced chronic hypertension are identically sustained by very small increases in plasma Ang II. Blood pressure increases more slowly with renin infusions, consistent with tissue binding. Notwithstanding, no evidence was obtained for a physiological role of tissue-bound renin in causing the cardiovascular, renal, hormonal and drinking responses measured in this study.
研究血浆血管紧张素II（Ang II）是否决定肾素-血管紧张素系统的作用，或者肾素的组织摄取及局部Ang II生成是否可解释循环肾素对心血管、肾脏、激素或饮水的影响。
在1周对照期后，将产生相似血浆Ang II水平的肾素（0.6 ng/分钟；n = 10）和Ang II（3.5 ng/分钟；n = 10）静脉输注到清醒大鼠体内，并与溶媒（n = 7）进行2周比较。连续测量平均动脉压（MAP）和心率。每周两次测量激素和肾功能。在另外7只大鼠中测量血浆Ang II和恢复数据。
在输注肾素和Ang II的大鼠中，血浆Ang II分别从4.5±0.8和4.4±0.9 pg/ml相似地增加到10.8±0.7和10.6±0.7 pg/ml，并在第二周相似地下降到7.0±1.1和7.0±1.5 pg/ml。血浆肾素分别从4.2±0.
