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肾内输注前列腺素期间的利钠机制。

Mechanism of natriuresis during intrarenal infusion of prostaglandins.

作者信息

Haas J A, Hammond T G, Granger J P, Blaine E H, Knox F G

出版信息

Am J Physiol. 1984 Sep;247(3 Pt 2):F475-9. doi: 10.1152/ajprenal.1984.247.3.F475.

DOI:10.1152/ajprenal.1984.247.3.F475
PMID:6476124
Abstract

Intrarenal infusion of the natural prostaglandin PGE2 increases renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. A newly synthesized prostaglandin analogue, 4-3-[3-[2-(1-hydroxycyclohexyl)- ethyl]-4-oxo-2-thiazolidinyl]propyl benzoic acid, increases renal blood flow without increasing sodium excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation, comparisons were made between PGE2 and the prostaglandin analogue. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. Following a similar increase in renal blood flow with intrarenal infusion of prostaglandin analogue, renal interstitial hydrostatic pressure and urinary sodium excretion were not changed. To determine whether increases in urinary sodium excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary sodium excretion did not change although there was a marked increase in renal blood flow. We conclude that increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary sodium excretion with prostaglandin-mediated renal vasodilation.

摘要

肾内输注天然前列腺素PGE2可增加肾血流量、肾间质静水压和尿钠排泄。一种新合成的前列腺素类似物,4-3-[3-[2-(1-羟基环己基)-乙基]-4-氧代-2-噻唑烷基]丙基苯甲酸,可增加肾血流量而不增加钠排泄。为了研究肾间质静水压在这种解离中的作用,对PGE2和前列腺素类似物进行了比较。肾内输注PGE2可增加肾血流量、肾间质静水压和尿钠排泄。在肾内输注前列腺素类似物使肾血流量有类似增加后,肾间质静水压和尿钠排泄未发生变化。为了确定PGE2输注导致的尿钠排泄增加是否与肾间质静水压升高有因果关系,而非与肾血流量增加有关,在间质压力未升高的情况下获得了对PGE2的反应。当肾间质静水压保持恒定时,尽管肾血流量显著增加,但尿钠排泄并未改变。我们得出结论,在前列腺素介导的肾血管舒张过程中,肾间质静水压升高是尿钠排泄增加所必需的。

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