Aukland K, Oien A H
Am J Physiol. 1987 Apr;252(4 Pt 2):F768-83. doi: 10.1152/ajprenal.1987.252.4.F768.
As shown previously, autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR) at varying arterial pressure may result from a myogenic response (MR) acting to maintain wall tension in each preglomerular vessel segment. We now combine MR with tubuloglomerular feedback (TGF) responding to distal tubular flow rate. The model consists of preglomerular and postglomerular resistances, glomerular filtration, and a tubular system. TGF acting on preglomerular resistance with parameters that mimic responses to single nephron distal tubular flow rate in rats and dogs failed to account for the autoregulation of RBF and GFR observed experimentally. Good autoregulation was obtained by adding preglomerular MR. In this combination, TGF is activated mainly in the lower range of autoregulation. Addition of mechanisms that increase postglomerular resistance or increase the glomerular filtration coefficient at reduced arterial pressure impairs RBF autoregulation, whereas GFR autoregulation is only slightly improved. TGF regulation of pre- and postglomerular resistance in the same direction seems compatible with good autoregulation only when combined with a preglomerular myogenic mechanism.
如前所示,在不同动脉压下肾血流量(RBF)和肾小球滤过率(GFR)的自身调节可能源于肌源性反应(MR),该反应作用于维持每个肾小球前血管段的壁张力。我们现在将MR与对远曲小管流速作出反应的管球反馈(TGF)相结合。该模型由肾小球前和肾小球后阻力、肾小球滤过以及一个肾小管系统组成。TGF作用于肾小球前阻力,其参数模拟大鼠和狗单个肾单位远曲小管流速的反应,但未能解释实验中观察到的RBF和GFR的自身调节。通过加入肾小球前MR可实现良好的自身调节。在这种组合中,TGF主要在自身调节的较低范围内被激活。在动脉压降低时增加肾小球后阻力或增加肾小球滤过系数的机制会损害RBF自身调节,而GFR自身调节仅略有改善。仅当与肾小球前肌源性机制相结合时,TGF对肾小球前和肾小球后阻力的同向调节似乎才与良好的自身调节相容。