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肾内肾小管液减弱心房钠尿肽诱导的球管反馈抑制。

Native tubular fluid attenuates ANF-induced inhibition of tubuloglomerular feedback.

作者信息

Pollock D M, Arendshorst W J

机构信息

Department of Physiology, University of North Carolina, Chapel Hill School of Medicine 27599-7545.

出版信息

Am J Physiol. 1990 Jan;258(1 Pt 2):F189-98. doi: 10.1152/ajprenal.1990.258.1.F189.

Abstract

The effect of atrial natriuretic factor [ANF-(1-28); 0.25 microgram.kg-1.min-1] on tubuloglomerular feedback (TGF) and the efficiency of renal blood flow (RBF) autoregulation was determined in anesthetized euvolemic rats. In microperfusion studies, ANF dramatically inhibited (greater than 80%) feedback-mediated decreases in single-nephron glomerular filtration rate (SNGFR) and stop-flow pressure (Psf) when Henle's loop was perfused at 0-48 nl/min with artificial fluid. The sigmoidal relationship between Psf and loop perfusion during control was shifted to a linear relation during ANF; reactivity was almost nonexistent and no inflection point could be discerned. ANF almost completely blocked maximum Psf and SNGFR responses to loop perfusion at rates greater than 24 nl/min. In contrast 30 nl/min loop perfusion with native proximal tubular fluid obtained during ANF infusion restored maximum TGF activity to 70% of control levels. During ANF administration, the paired Psf responses to native and artificial perfusate were significantly different (-5.3 vs. -0.8 mmHg, P less than 0.001), compared with similar responses during control conditions (-7.6 vs. -8.3 mmHg, P greater than 0.1). In free-flow studies, ANF increased proximally and distally measured SNGFR equally. The constancy of the proximal-distal SNGFR difference (10.3 vs. 9.3 nl/min) in the presence of increased distal fluid delivery suggests partial inhibition of TGF during ANF administration. ANF elevated Psf but did not affect basal RBF or the RBF autoregulatory index over an arterial pressure range of 130-70 mmHg. These results indicate that 1) RBF autoregulation is efficiently maintained during ANF infusion when preglomerular vessels are vasodilated and TGF is inhibited by approximately 30%; 2) an endogenous factor(s) in native proximal tubular fluid may attenuate ANF-induced inhibition of TGF; and 3) microperfusion studies using artificial fluid significantly overestimate the net in vivo effect of ANF on TGF.

摘要

在麻醉的血容量正常大鼠中,测定了心房利钠因子[ANF-(1 - 28);0.25微克·千克⁻¹·分钟⁻¹]对肾小管-肾小球反馈(TGF)和肾血流量(RBF)自身调节效率的影响。在微灌注研究中,当以0 - 48纳升/分钟的速度用人工液体灌注亨利氏袢时,ANF显著抑制(大于80%)反馈介导的单肾单位肾小球滤过率(SNGFR)和停流压力(Psf)的降低。对照期间Psf与袢灌注之间的S形关系在ANF作用期间转变为线性关系;反应性几乎不存在,无法辨别拐点。当袢灌注速度大于24纳升/分钟时,ANF几乎完全阻断了Psf和SNGFR对袢灌注的最大反应。相比之下,在输注ANF期间用天然近端小管液以30纳升/分钟的速度进行袢灌注可使最大TGF活性恢复至对照水平的70%。在给予ANF期间,与对照条件下的类似反应(-7.6对-8.3 mmHg,P大于0.1)相比,对天然和人工灌注液的配对Psf反应显著不同(-5.3对-0.8 mmHg,P小于0.001)。在自由流研究中,ANF使近端和远端测量的SNGFR同等增加。在远端液体输送增加的情况下,近端-远端SNGFR差值的恒定(10.3对9.3纳升/分钟)表明在给予ANF期间TGF受到部分抑制。ANF使Psf升高,但在130 - 70 mmHg的动脉压范围内不影响基础RBF或RBF自身调节指数。这些结果表明:1)当肾小球前血管舒张且TGF被抑制约30%时,在输注ANF期间RBF自身调节得以有效维持;2)天然近端小管液中的一种内源性因子可能减弱ANF诱导的TGF抑制作用;3)使用人工液体的微灌注研究显著高估了ANF对TGF的体内净效应。

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