Iversen B M, Kvam F I, Matre K, Ofstad J
Renal Research Group, Medical Department A, University of Bergen, N-5021 Bergen, Norway.
Am J Physiol. 1998 Aug;275(2):R343-9. doi: 10.1152/ajpregu.1998.275.2.R343.
Decrease in systemic blood pressure, duration of pressure decrease, and change in the activity of the renin or the sympathetic nervous system may represent mechanisms involved in resetting the renal blood flow (RBF) autoregulation found in hypertensive rats. Autoregulation of RBF, plasma renin concentration (PRC), and the time needed for resetting to take place were studied in the nonclipped kidney before and after removal of the clipped kidney of two- kidney, one-clip (2K1C) hypertensive rats and before and after mechanical reduction of the renal arterial pressure (RAP) for 10 min in the spontaneously hypertensive rat (SHR) and in the nonclipped kidney of 2K1C hypertensive rats with and without renal denervation. Mean arterial pressure (MAP) fell from 147 to 107 mmHg 30 min after removal of the clipped kidney, and the lower pressure limit of RBF autoregulation decreased from 113 to 90 mmHg (P < 0.01); PRC fell. Mechanical reductions of RAP from 161 to 120 mmHg in the nonclipped kidney for 10 min did not change RBF, but at 120 mmHg, the lower pressure limit of RBF autoregulation was reduced from 115 mmHg before pressure reduction to 96 mmHg afterwards (P < 0.02). In SHR, similar pressure reduction for 10 min decreased the lower pressure limit of RBF autoregulation from 106 to 86 mmHg (P < 0.01). PRC was unchanged in both models, and denervation did not change RBF autoregulation. When RAP was reduced below the lower pressure limit of RBF autoregulation, RBF decreased approximately 20%; the lower pressure limit of RBF autoregulation remained unchanged. In normotensive Wistar-Kyoto rats, pressure reduction did not change the range of RBF autoregulation. These results indicate that acute normalization of the pressure range of RBF autoregulation in hypertensive rats is dependent on the degree of pressure reduction of RAP, whereas renal innervation and PRC do not play a major role. We propose that the mechanism of resetting is due to afterstretch of noncontractile elements of the vessel wall or is caused by pure myogenic mechanisms. An effect of intrarenal angiotensin cannot be excluded.
全身血压的降低、血压降低的持续时间以及肾素或交感神经系统活性的变化，可能代表参与重置高血压大鼠肾血流量（RBF）自身调节的机制。在双肾单夹（2K1C）高血压大鼠切除夹闭肾之前和之后，以及在自发性高血压大鼠（SHR）和有或无肾去神经支配的2K1C高血压大鼠的非夹闭肾中，在机械降低肾动脉压（RAP）10分钟之前和之后，研究了RBF的自身调节、血浆肾素浓度（PRC）以及发生重置所需的时间。切除夹闭肾30分钟后，平均动脉压（MAP）从147 mmHg降至107 mmHg，RBF自身调节的下限压力从113 mmHg降至90 mmHg（P < 0.01）；PRC下降。在非夹闭肾中，将RAP从161 mmHg机械降低至120 mmHg并持续10分钟，并未改变RBF，但在120 mmHg时，RBF自身调节的下限压力从降压前的115 mmHg降至降压后的96 mmHg（P < 0.02）。在SHR中，类似的10分钟降压使RBF自身调节的下限压力从106 mmHg降至86 mmHg（P < 0.01）。在两种模型中PRC均未改变，且去神经支配并未改变RBF自身调节。当RAP降低至低于RBF自身调节的下限压力时，RBF下降约20%；RBF自身调节的下限压力保持不变。在正常血压的Wistar - Kyoto大鼠中，降压并未改变RBF自身调节的范围。这些结果表明，高血压大鼠中RBF自身调节压力范围的急性正常化取决于RAP的降压程度，而肾神经支配和PRC并不起主要作用。我们提出重置机制是由于血管壁非收缩成分的牵张后效应或由纯粹的肌源性机制引起。不能排除肾内血管紧张素的作用。
