Gotshall R, Hess T, Mills T
Blood Vessels. 1985;22(1):25-31.
In order to evaluate vascular (myogenic) and tubular (tubuloglomerular feedback) mechanisms involved in renal blood flow (RBF) autoregulation, canine kidneys with filtration (normal) and without filtration (nonfiltering, NFK; ureteral-obstructed, UO) were studied. RBF was monitored in response to stepwise reductions in renal perfusion pressure of -20, -40, and -60 mm Hg from control pressure. None of the three groups demonstrated significant changes in RBF from their respective control values (normal, 380 ml/min/100 g; NFK, 179 ml/min/100 g; UO, 153 ml/min/100 g) until the lowest pressure (-60 mm Hg from control pressure). All three groups responded to the pressure reductions with significant decreases in renal vascular resistance. However, the calculated efficiency of the autoregulatory response for the NFK and UO groups was significantly less than for the normal group. Elimination of tubuloglomerular feedback (NFK and UO) did not necessarily eliminate renal vascular autoregulation, but did reduce the efficiency of autoregulation. It is suggested that both vascular (myogenic) and tubular (tubuloglomerular) mechanisms may coexist to efficiently autoregulate blood flow in normal filtering kidneys. However, a reduction in metabolic activity as a contributor to the reduced ability to autoregulate in these kidneys could be an additional possibility.
为了评估参与肾血流量（RBF）自身调节的血管（肌源性）和肾小管（肾小管-肾小球反馈）机制，对具有滤过功能（正常）和无滤过功能（无滤过，NFK；输尿管梗阻，UO）的犬肾进行了研究。监测了RBF对肾灌注压从对照压力逐步降低-20、-40和-60 mmHg的反应。在最低压力（比对照压力低-60 mmHg）之前，三组中均未观察到RBF相对于各自对照值（正常，380 ml/min/100 g；NFK，179 ml/min/100 g；UO，153 ml/min/100 g）有显著变化。所有三组对压力降低的反应均表现为肾血管阻力显著降低。然而，计算得出的NFK组和UO组自身调节反应的效率显著低于正常组。消除肾小管-肾小球反馈（NFK和UO）并不一定会消除肾血管自身调节，但确实降低了自身调节的效率。提示血管（肌源性）和肾小管（肾小管-肾小球）机制可能共同存在，以有效地对正常滤过肾中的血流进行自身调节。然而，代谢活性降低作为这些肾脏自身调节能力降低的一个因素也可能是另一种可能性。
