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肾间质静水压对钠排泄的调节

Regulation of sodium excretion by renal interstitial hydrostatic pressure.

作者信息

Granger J P

出版信息

Fed Proc. 1986 Dec;45(13):2892-6.

PMID:3536586
Abstract

Renal interstitial hydrostatic pressure (RIHP) appears to play a crucial role in linking the renal circulation to the rate of tubular reabsorption of sodium and water. Various physiological and pharmacological maneuvers that increase RIHP are associated with increases in sodium excretion. Renal vasodilators that increase RIHP also increase sodium excretion, whereas the vasodilators that do not alter RIHP do not affect sodium excretion. Preventing increases in RIHP during intrarenal infusion of vasodilators markedly attenuates the normal increase in sodium and water excretion. Techniques that directly increase RIHP by renal interstitial volume expansion increase urinary excretion of sodium and water. RIHP may be an important mediator of renal perfusion pressure (RPP) natriuresis. Experimental evidence suggests that the proximal tubule of deep nephrons may be an important nephron site that is sensitive to changes in RPP.

摘要

肾间质静水压(RIHP)似乎在将肾循环与钠和水的肾小管重吸收率联系起来方面发挥着关键作用。各种增加RIHP的生理和药理操作都与钠排泄增加有关。增加RIHP的肾血管扩张剂也会增加钠排泄,而不改变RIHP的血管扩张剂则不会影响钠排泄。在肾内输注血管扩张剂期间防止RIHP升高可显著减弱钠和水排泄的正常增加。通过肾间质容积扩张直接增加RIHP的技术会增加钠和水的尿排泄。RIHP可能是肾灌注压(RPP)利钠作用的重要介质。实验证据表明,深部肾单位的近端小管可能是对RPP变化敏感的重要肾单位部位。

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