Marsh D J
Kidney Int Suppl. 1982 Aug;12:S165-72.
To estimate the frequency response of autoregulation and to test whether macula densa feedback alone mediates renal blood flow (RBF) autoregulation in rats, we imposed sudden increases (10 to 20 mm Hg) in arterial pressure (AP) and compared the time courses of renal vascular resistance (RVR) changes and of flow changes at the macula densa. RVR decreased abruptly after the AP increase, but returned to control levels in less than 1 sec, continued to increase, reaching 50% completion within 3 sec, and achieved final values 15 to 20 sec after AP change. To predict transient changes in tubule flow, we derived a model of pressure and flow and combined it with measurements of tubule pressure made during AP steps. With these measured pressures as inputs, the model predicted a prompt rise in GFR followed by a decline that returned GFR halfway to control values within 3 to 4 sec and more slowly thereafter. Predicted early distal flow increased perceptibly only after 1 sec and rose slowly thenceforth. The disturbance in early distal flow appears to arrive too late to signal the rapid changes in RVR. Some other mechanism, possibly myogenic, must have intervened. The results suggest that two mechanisms mediate autoregulation, each with a different response time. The putative myogenic mechanism is about one order of magnitude faster than the macula densa.
为了估计自身调节的频率响应，并测试是否仅致密斑反馈介导大鼠肾血流量（RBF）自身调节，我们突然提高动脉压（AP）10至20 mmHg，并比较肾血管阻力（RVR）变化和致密斑处血流变化的时间过程。AP升高后RVR立即下降，但在不到1秒内恢复到对照水平，继续升高，在3秒内达到50%的变化量，并在AP变化后15至20秒达到最终值。为了预测肾小管流量的瞬时变化，我们推导了一个压力和流量模型，并将其与AP阶跃期间测量的肾小管压力相结合。以这些测量压力作为输入，该模型预测肾小球滤过率（GFR）迅速上升，随后下降，在3至4秒内使GFR降至对照值的一半，此后下降更缓慢。预测的早期远端流量仅在1秒后才明显增加，此后缓慢上升。早期远端流量的干扰似乎来得太晚，无法为RVR的快速变化发出信号。一定有其他机制，可能是肌源性机制，进行了干预。结果表明，两种机制介导自身调节，每种机制具有不同的响应时间。假定的肌源性机制比致密斑快约一个数量级。
