Increased tubular flow induces resetting of tubuloglomerular feedback in euvolemic rats.

Increased tubular flow induces resetting of tubuloglomerular feedback in euvolemic rats.
复制标题

DOI:
10.1152/ajprenal.1996.270.3.f461
复制
发表时间:
1996-03
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
S. Thomson;R. Blantz;V. Vallon
S. Thomson;R. Blantz;V. Vallon
中科院分区:
其他
文献类型:
--
作者:
S. Thomson;R. Blantz;V. Vallon

文献摘要

被引文献

相似文献

随着单肾单位肾小球滤过率 (SNGFR) 和晚期近端流量 (VLP) 在生长过程中或体积扩张后增加,肾小球反馈 (TGF) 功能(定义为由于 TGF 过程导致的 SNGFR 减少)在由 VLP 和 SNGFR 定义的平面中向右移动,以维持 TGF 的稳态效率。目前尚不清楚 TGF 的这种重置是否需要全身激素环境的变化,还是 TGF 本身长期激活的结果。我们采用微穿刺和视频流速测定法(一种测量畅通肾单位血流的光学技术)来解决 Inactin 麻醉的正常血容量大鼠中的这个问题。在通过向早期近端流量 (VEP) 添加 20 nl/min 施加的流量持续增加之前和期间,反复评估 TGF 对 VLP 中扰动 [晚期近端流量扰动 (VH) = +/- 5 nl/min] 的分数补偿 (C)。增加VEP最初使TGF饱和,从而抑制C。在接下来的30分钟内,C恢复到其原始值的70%,表明TGF功能向右重置以匹配VLP的增加。通过以 4 nl/min 的增量测试 C 与 VH 的 -12 < 或 = VH < 或 = 12,记录 C 关于 VH = 0 的不对称性的演变,从而确认重置。增强 VEP 超过 30 分钟后,由于 TGF 脱敏,C 值逐渐下降。 VLP 的持续增加足以包括 TGF 的重置,与全身神经体液环境的任何变化无关。
As single-nephron glomerular filtration rate (SNGFR) and late proximal flow (VLP) increase during growth or following volume expansion, the tubuloglomerular feedback (TGF) function (defined as the decrement in SNGFR due to the process of TGF) shifts rightward in the plane defined by VLP and SNGFR as required to maintain the homeostatic efficiency of TGF. It is not known whether this resetting of TGF requires changes in the systemic hormonal milieu or results from prolonged activation of TGF itself. We employed micropuncture and videometric flow velocitometry (an optical technique for measuring flow in unobstructed nephrons) to address this issue in Inactin-anesthetized euvolemic rats. The fractional compensation (C) of TGF for perturbations [late proximal flow perturbation (VH) = +/- 5 nl/min] in VLP was assessed repeatedly before and during a sustained increase in flow imposed by adding 20 nl/min to early proximal flow (VEP). Augmenting VEP initially saturated TGF, thus suppressing C. Over the next 30 min, C recovered to 70% of its original value, suggesting a rightward resetting of the TGF function to match the increase imposed on VLP. Resetting was confirmed by documenting an evolving asymmetry of C about VH = 0 by testing C vs. VH for -12 < or = VH < or = 12 in increments of 4 nl/min. Beyond 30 min of augmented VEP, C gradually declined due to desensitization of TGF. A sustained increase in VLP is sufficient to include TGF resetting, independent of any change in the systemic neurohumoral milieu.