Navar L G, Saccomani G, Mitchell K D
Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana.
Am J Hypertens. 1991 Jan;4(1 Pt 1):90-6. doi: 10.1093/ajh/4.1.90.
There is a growing awareness that the direct intrarenal actions of angiotensin II (ANG II) on both tubular and vascular structures contribute to sodium conservation. Even very low concentrations of ANG II (10(-1)) mol/L) stimulate proximal reabsorption rate. Recent studies indicate that this stimulatory action is due to an enhanced activity of the sodium/hydrogen exchanger of the luminal membrane. Elevated ANG II levels in the renal interstitium, effected either through increased delivery of ANG II via the circulation or as a consequence of conversion of angiotensin I (ANG I) generated locally, can also enhance proximal reabsorption rate. One consequence of enhanced proximal reabsorption rate is reduced distal volume delivery, which would be expected to elicit arteriolar vasodilation mediated by the tubuloglomerular feedback (TGF) mechanism. It has been observed, however, that peritubular capillary infusions of either ANG I or ANG II, at doses sufficiently low to be without obvious direct effects on glomerular dynamics, can increase the sensitivity of the TGF mechanism. This enhanced TGF sensitivity serves to minimize or prevent TGF mediated increases in glomerular filtration rate in the face of reduced distal delivery. With greater increases in interstitial ANG II concentration, reductions in glomerular pressure have been observed, demonstrating a powerful action on preglomerular arterioles that predominates over the well known effects on efferent arterioles. At these higher doses, the direct hemodynamic actions of ANG II, plus the effects on the glomerular filtration coefficient, will directly reduce filtered sodium load. Through these synergistic effects on both tubular reabsorptive and hemodynamic function, ANG II can elicit sustained decreases in distal nephron sodium delivery which contribute greatly to its efficacy as a regulator of sodium excretion.
人们越来越意识到，血管紧张素II（ANG II）对肾小管和血管结构的直接肾内作用有助于钠的潴留。即使是非常低浓度的ANG II（10^(-11)mol/L）也能刺激近端重吸收率。最近的研究表明，这种刺激作用是由于管腔膜钠/氢交换器的活性增强。肾间质中ANG II水平升高，无论是通过循环中ANG II输送增加还是局部产生的血管紧张素I（ANG I）转化的结果，也能提高近端重吸收率。近端重吸收率提高的一个后果是远端容量输送减少，这有望引发由管球反馈（TGF）机制介导的小动脉血管舒张。然而，已经观察到，以足够低的剂量向肾小管周围毛细血管输注ANG I或ANG II，使其对肾小球动力学无明显直接影响，可增加TGF机制的敏感性。这种增强的TGF敏感性有助于在远端输送减少的情况下最小化或防止TGF介导的肾小球滤过率增加。随着间质ANG II浓度的进一步增加，已观察到肾小球压力降低，这表明对入球小动脉有强大作用，其作用超过了对出球小动脉的众所周知的作用。在这些较高剂量下，ANG II的直接血流动力学作用加上对肾小球滤过系数的影响，将直接降低滤过钠负荷。通过对肾小管重吸收和血流动力学功能的这些协同作用，ANG II可引起远端肾单位钠输送的持续减少，这对其作为钠排泄调节剂的功效有很大贡献。
