Importance of efferent arteriolar vascular tone in regulation of proximal tubule fluid reabsorption and glomerulotubular balance in the rat.
Importance of efferent arteriolar vascular tone in regulation of proximal tubule fluid reabsorption and glomerulotubular balance in the rat.
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传出小动脉血管张力在调节大鼠近端肾小管液体重吸收和肾小球小管平衡中的重要性。
DOI：
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发表时间：
1980
影响因子：
15.9
通讯作者：
B. Brenner
中科院分区：
文献类型：
--
作者：
I. Ichikawa;B. Brenner
在21只轻度扩容的Munich-Wistar大鼠中进行部分主动脉缩窄之前和期间的微穿刺研究，以检查内源性前列腺素（PG）和血管紧张素II（AII）对单肾单位肾小球滤过率（SNGFR）和绝对近端重吸收率（APR）的影响。动物接受媒介物（第1组）、吲哚美辛（第2组）或吲哚美辛加萨拉拉辛（第3组）。主动脉缩窄前，这些抑制剂对 SNGFR 和 APR 值没有影响。在第 1 组大鼠中，平均肾动脉灌注压 (RAP) 降低至约 65 mm Hg 导致 SNGFR 和 APR 显着成比例下降。然而，随着第 2 组大鼠 RAP 的同等减少，SNGFR 下降的程度较小，而 APR 往往略高于收缩前的值。因此，吲哚美辛的施用与肾小球小管平衡的破坏有关。鉴于第 1 组和第 2 组测量的传入小动脉阻力大致相同的下降，传出小动脉阻力 (R(E)) 增加的幅度似乎对于确定观察到的肾小球小管平衡是否存在具有重要意义。因此，第 2 组中的 SNGFR 下降幅度小于第 1 组，这是第 2 组中肾小球毛细血管液压值较高的结果，而第 2 组中的肾小球毛细血管液压值较高，这是 R(E) 值较高的结果。第 2 组 RAP 降低期间 APR 平均值高于第 1 组，这也可归因于 R(E) 的显着升高，其作用是通过有利于更高的肾小球后胶体渗透压和更低的下游（肾小管周围毛细血管）液压来增加净重吸收压力。由于当 RAP 下降时 AII 的肾内释放增强，并且已知 AII 会选择性地升高 R(E)，因此内源性 AII 很可能导致第 2 组中 R(E) 显着增加，这仅在吲哚美辛治疗的大鼠中很容易证明，可能是因为内源性 PG 合成受到抑制。与这一结论一致，当第3组大鼠中saralasin抑制内源性AII的作用时，RAP的减少未能引起R(E)的升高，因此净滤过和重吸收压力再次成比例下降，SNGFR和APR也是如此。因此，目前的证据表明，肾小球小管平衡在很大程度上受到传出小动脉的血管舒缩张力的影响。
Micropuncture study was performed in 21 mildly volume-expanded Munich-Wistar rats before and during partial aortic constriction to examine the effects of endogenous prostaglandins (PG) and angiotensin II (AII) on single nephron glomerular filtration rate (SNGFR) and absolute proximal reabsorption rate (APR). Animals received either vehicle (group 1), indomethacin (group 2), or indomethacin plus saralasin (group 3). Before aortic constriction, these inhibitors were without effect on values of SNGFR and APR. In group 1 rats, reduction in mean renal arterial perfusion pressure (RAP) to approximately 65 mm Hg resulted in marked and proportional declines in SNGFR and APR. With equivalent reduction in RAP in group 2 rats, however, SNGFR fell to a lesser extent and APR tended to increase slightly above preconstriction values. Indomethacin administration was therefore associated with disruption of glomerulotubular balance. In view of the roughly equivalent declines in afferent arteriolar resistance measured in groups 1 and 2, the magnitude of increase in efferent arteriolar resistance (R(E)) appeared to be of major importance in determining the observed presence or absence of glomerulotubular balance. Thus, the lesser fall in SNGFR in group 2 than in group 1 was a result of the higher value for glomerular capillary hydraulic pressure in group 2, a consequence of the higher value of R(E). The higher average value for APR during reduced RAP in group 2 than in group 1 is also attributable to this pronounced rise in R(E), the effect of which was to augment the net reabsorptive pressure both by favoring higher postglomerular oncotic pressure and lower downstream (peritubular capillary) hydraulic pressure. Since intrarenal release of AII is enhanced when RAP declines, and because AII is known to raise R(E) selectively, it is likely that endogenous AII brought about the marked increase in R(E) in group 2, which was readily demonstrable only in indomethacin-treated rats, presumably because endogenous PG synthesis was suppressed. In keeping with this conclusion, when the action of endogenous AII was inhibited by saralasin in group 3 rats, reduction in RAP failed to induce a rise in R(E), so that net filtration and reabsorption pressures again declined proportionally, as did SNGFR and APR. The present evidence therefore suggests that glomerulotubular balance is influenced to an important extent by the prevailing vasomotor tone of the efferent arteriole.