EFFECT OF CAPTOPRIL ON FLUCTUATIONS OF BLOOD-PRESSURE AND RENAL BLOOD-FLOW IN RATS

被引:23
作者
HE, JC
MARSH, DJ
机构
[1] UNIV HEIDELBERG, INST PHYSIOL 1, W-6900 HEIDELBERG, GERMANY
[2] UNIV SO CALIF, SCH MED, DEPT PHYSIOL & BIOPHYS, LOS ANGELES, CA 90033 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 264卷 / 01期
关键词
ANGIOTENSIN-II; AUTOREGRESSIVE MODELS; AUTOREGRESSIVE-MOVING AVERAGE MODELS; FREQUENCY DOMAIN ANALYSIS; RENAL DYNAMICS; TUBULOGLOMERULAR FEEDBACK;
D O I
10.1152/ajprenal.1993.264.1.F37
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Arterial blood pressure and renal blood flow (RBF) fluctuations in rats were studied by autoregressive (AR) and autoregressive-moving average (ARMA) modeling. These estimation procedures provided greater sensitivity and frequency resolution than classic fast Fourier transform (FFT)-based methods and also require shorter observation periods. We estimated the transfer function of RBF autoregulation to test whether inhibition of angiotensin-converting enzyme impairs whole kidney dynamic autoregulation. The transfer function in control animals measured with the ARMA method was similar to transfer functions obtained previously, using FFT methods. Because of better frequency resolution, we also detected an oscillation in RBF at 50 mHz, the same frequency as an oscillation in tubular pressure and glomerular filtration rate that had been attributed to tubuloglomerular feedback (TGF), but that FFT methods had not previously found in whole kidney blood flow. Captopril increased the amplitude of RBF fluctuations and increased the gain of the transfer function at frequencies below 100 mHz, a frequency bandwidth previously associated with TGF. The increased gain indicates that TGF operates less effectively to mediate dynamic autoregulation when angiotensin conversion is inhibited. Gain at frequencies greater than 100 mHz, previously ascribed to the myogenic mechanism, was not affected by captopril. These results show that angiotensin, by modulating TGF, reduces fluctuations of RBF about the mean value.
引用
收藏
页码:F37 / F44
页数:8
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