Moore L C, Schnermann J, Yarimizu S
Am J Physiol. 1979 Jul;237(1):F63-74. doi: 10.1152/ajprenal.1979.237.1.F63.
Tubuloglomerular feedback (TGF) mediation of autoregulation was investigated by measuring the response of single nephron glomerular filtration rate (SNGFR) to changes in arterial pressure (AP) following acute or chronic TGF inhibition. In hydropenic rats with intact TGF, distal SNGFR was 25.0 +/- 1.2 (SE) and 23.9 +/- 1.4 nl/min at AP of 111 and 135 mmHg, respectively. In the same 20 nephrons during proximal tubular microinfusion of furosemide, distal SNGFR was 23.6 +/- 1.4 (n = 16) and 29.7 +/- 1.4 nl/min (n = 20) (P less than 0.001, n = 16) at 112 and 133 mmHg. When determined proximally, SNGFR was 25.6 +/- 1.0 and 29.5 +/- 0.9 nl/min (P less than 0.001, n = 31) at 112 and 157 mmHg; kidney GFR increased similarly. These data and the predictions of a GFR model were then used to estimate autoregulatory efficiency. This analysis indicated that partial autoregulation occurred during TGF inhibition. Therefore, TGF is an essential, but probably not the only, mechanism mediating SNGFR autoregulation.
通过测量急性或慢性肾小管-肾小球反馈（TGF）抑制后单个肾单位肾小球滤过率（SNGFR）对动脉压（AP）变化的反应，研究了TGF介导的自身调节。在TGF完整的缺水大鼠中，在111和135 mmHg的AP下，远端SNGFR分别为25.0±1.2（SE）和23.9±1.4 nl/min。在相同的20个肾单位中，在近端肾小管微量注入呋塞米期间，在112和133 mmHg时，远端SNGFR分别为23.6±1.4（n = 16）和29.7±1.4 nl/min（n = 20）（P<0.001，n = 16）。当在近端测定时，在112和157 mmHg时，SNGFR分别为25.6±1.0和29.5±0.9 nl/min（P<0.001，n = 31）；肾脏GFR也有类似增加。然后，这些数据和GFR模型的预测被用于估计自身调节效率。该分析表明，在TGF抑制期间发生了部分自身调节。因此，TGF是介导SNGFR自身调节的一种重要机制，但可能不是唯一的机制。
