Wende P, Strauch M, Unger T, Gretz N, Rohmeiss P
Nephrologische Klinik, Klinikum der Stadt Mannheim.
Med Klin (Munich). 1993 Apr 15;88(4):207-11.
The autoregulation of renal blood flow (RBF), glomerular filtration rate (GFR) and the pressure dependent renin release into the circulation were studied in conscious chronically instrumented spontaneously hypertensive rats (SHR) and normotensive Wistar rats. Renal perfusion pressure was lowered by means of a suprarenal inflatable cuff on the abdominal aorta and was lowered in pressure steps of 10 mm Hg. Breakoff points for RBF- and GFR-autoregulation as well as the threshold for renin release were calculated using non-linear regression (breakpoint analysis). Wistar rats autoregulated RBF and GFR in a range between 110 and 90 mm Hg (breakoff points: RBF 88 +/- 2 mm Hg; GFR 92 +/- 3 mm Hg). Plasma-renin activity (PRA) showed a threshold of activation at 89 +/- 8 mm Hg. Breakoff points and threshold of renin release did not differ significantly from each other. SHR autoregulated RBF and GFR in a range between 160 and 100 mm Hg (breakoff points: RBF 104 +/- 6 mm Hg; GFR 99 +/- 4 mm Hg). The PRA increase had a threshold at 119 +/- 6 mm Hg. Breakoff points of RBF- and GFR-autoregulation did not differ significantly. In SHR the threshold of renin release was at a significantly higher pressure than the breakoff point of GFR-autoregulation. The comparison between Wistar rats and SHR revealed a significant shift of the RBF-autoregulation curve and the pressure-dependent renin release of SHR towards higher pressures (p < 0.05). The early increase of PRA in SHR suggests a role of the renin-angiotensin-system (RAS) in the autoregulation of GFR in SHR. Wistar rats seem to autoregulate GFR independently of the RAS. An activation of the sympathetic nervous system might take part in the rightward shift of the RBF- and GFR-autoregulation curve in SHR. The role of this altered autoregulatory pattern in the development of genetic hypertension remains to be investigated.
在清醒的、长期植入仪器的自发性高血压大鼠(SHR)和正常血压的Wistar大鼠中,研究了肾血流量(RBF)、肾小球滤过率(GFR)的自动调节以及压力依赖性肾素释放进入循环的情况。通过在腹主动脉上放置一个肾上腺充气袖带降低肾灌注压,并以10 mmHg的压力步长降低。使用非线性回归(断点分析)计算RBF和GFR自动调节的断点以及肾素释放的阈值。Wistar大鼠在110至90 mmHg的范围内自动调节RBF和GFR(断点:RBF 88±2 mmHg;GFR 92±3 mmHg)。血浆肾素活性(PRA)在89±8 mmHg时显示出激活阈值。肾素释放的断点和阈值彼此之间没有显著差异。SHR在160至100 mmHg的范围内自动调节RBF和GFR(断点:RBF 104±6 mmHg;GFR 99±4 mmHg)。PRA升高的阈值为119±6 mmHg。RBF和GFR自动调节的断点没有显著差异。在SHR中,肾素释放的阈值显著高于GFR自动调节的断点。Wistar大鼠和SHR之间的比较显示,SHR的RBF自动调节曲线和压力依赖性肾素释放显著向更高压力偏移(p<0.05)。SHR中PRA的早期升高表明肾素-血管紧张素系统(RAS)在SHR的GFR自动调节中起作用。Wistar大鼠似乎独立于RAS自动调节GFR。交感神经系统的激活可能参与了SHR中RBF和GFR自动调节曲线的右移。这种改变的自动调节模式在遗传性高血压发展中的作用仍有待研究。