Ichikawa I
Kidney Int Suppl. 1982 Aug;12:S109-13.
The current notion that tubuloglomerular feedback-mediated regulation of GFR involves selective changes in afferent arteriolar vasomotor tone stems from the familiar finding that manipulation of distal salt delivery alters glomerular capillary hydraulic pressure (PGC). Stop-flow technique, which has been used for this PGC measurement, however, has recently been shown to fail to provide a reliable estimate of true PGC. In the present study, glomerular dynamics were examined by direct glomerular puncture during loop perfusion with Ringer solution at rates of 0 and 40 nl/min. With the increased loop flow, single nephron GFR (SNGFR) decreased by approximately 35%. Because directly measured PGC remained unchanged, this reduction in SNGFR was due to the falls in glomerular plasma flow rate and ultrafiltration coefficient, the former a consequence of increases in both afferent and efferent arteriolar resistances. By contrast, PGC values estimated by the stop-flow technique declined substantially with increased loop flow. These results indicate that tubuloglomerular feedback-induced regulation of GFR is mediated by changes in the vasomotor tone of preglomerular, glomerular, and postglomerular vessels. In view of the close anatomical contact between mesangial cells and these vessels, mesangial contractility may play a role as the single effector mechanism regulating the vasomotor tone of these vessels.
目前关于管球反馈介导的肾小球滤过率(GFR)调节涉及入球小动脉血管舒缩张力选择性变化的观点,源于一个常见的发现,即对远曲小管盐转运的操作会改变肾小球毛细血管液压(PGC)。然而,用于测量该PGC的停流技术最近已被证明无法提供对真实PGC的可靠估计。在本研究中,在以0和40 nl/min的速率用林格液进行髓袢灌注期间,通过直接肾小球穿刺检查肾小球动力学。随着髓袢流量增加,单肾单位GFR(SNGFR)降低了约35%。由于直接测量的PGC保持不变,SNGFR的这种降低是由于肾小球血浆流速和超滤系数下降,前者是入球和出球小动脉阻力增加的结果。相比之下,通过停流技术估计的PGC值随着髓袢流量增加而大幅下降。这些结果表明,管球反馈诱导的GFR调节是由球前、球内和球后血管的血管舒缩张力变化介导的。鉴于系膜细胞与这些血管之间紧密的解剖学接触,系膜收缩性可能作为调节这些血管血管舒缩张力的单一效应机制发挥作用。