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饮食钠和遗传背景对小鼠血管紧张素原和肾素的影响。

Effects of dietary sodium and genetic background on angiotensinogen and Renin in mouse.

作者信息

Lantelme Pierre, Rohrwasser Andreas, Gociman Barbu, Hillas Elaine, Cheng Tong, Petty Gray, Thomas Jennifer, Xiao Sha, Ishigami Tomoaki, Herrmann Tracy, Terreros Daniel A, Ward Kenneth, Lalouel Jean-Marc

机构信息

Department of Human Genetics, University of Utah Health Sciences Center, Salt Lake City, USA.

出版信息

Hypertension. 2002 May;39(5):1007-14. doi: 10.1161/01.hyp.0000016177.20565.a0.

DOI:10.1161/01.hyp.0000016177.20565.a0
PMID:12019284
Abstract

Elements of a renin-angiotensin system expressed along the entire nephron, including angiotensinogen secreted by proximal tubule and renin expressed in connecting tubule, may participate in the regulation of sodium reabsorption at multiple sites of the nephron. The response of this tubular renin-angiotensin system to stepwise changes in dietary sodium was investigated in 2 mouse strains, the sodium-sensitive inbred C57BL/6 and the sodium-resistant CD1 outbred. Plasma angiotensinogen was not affected by sodium regimen, whereas plasma renin increased 2-fold under low sodium. In both strains, the variation in urinary parameters did not parallel the changes observed in plasma. Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Water deprivation, by contrast, induced significant activation in the tubular expression of angiotensinogen and renin. C57BL/6 exhibited significantly higher urinary excretion of angiotensinogen than did CD1 animals under both conditions of sodium intake. The extent to which these urinary parameters reflect systemic or tubular responses to challenges of sodium homeostasis may depend on the relative contribution of sodium restriction and volume depletion.

摘要

整个肾单位均表达肾素 - 血管紧张素系统的成分,包括近端小管分泌的血管紧张素原和连接小管表达的肾素,它们可能参与肾单位多个部位钠重吸收的调节。在两种小鼠品系中研究了这种肾小管肾素 - 血管紧张素系统对饮食中钠逐步变化的反应,即钠敏感的近交系C57BL/6和钠抵抗的远交系CD1。血浆血管紧张素原不受钠摄入方案的影响,而血浆肾素在低钠情况下增加2倍。在两个品系中,尿参数的变化与血浆中观察到的变化并不平行。高钠时血管紧张素原和肾素排泄显著高于低钠时。相反,禁水诱导血管紧张素原和肾素的肾小管表达显著激活。在两种钠摄入情况下,C57BL/6的血管紧张素原尿排泄均显著高于CD1动物。这些尿参数反映全身或肾小管对钠稳态挑战反应的程度可能取决于钠限制和容量耗竭的相对作用。

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