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高血压早期发展过程中的N-ε-(羧甲基)赖氨酸

N epsilon-(carboxymethyl)lysine during the early development of hypertension.

作者信息

Baumann Marcus, Stehouwer Coen, Scheijen Jean, Heemann Uwe, Struijker Boudier Harry, Schalkwijk Casper

机构信息

Department of Pharmacology and Toxicology, University Maastricht, Maastricht, the Netherlands.

出版信息

Ann N Y Acad Sci. 2008 Apr;1126:201-4. doi: 10.1196/annals.1433.004. Epub 2007 Dec 13.

Abstract

Advanced glycation end products (AGEs) are associated with hypertension. Whether N(epsilon)-(carboxymethyl)lysine (CML) contributes to the development of hypertension in young spontaneously hypertensive rats (SHR) remains to be established compared to WKY. We determined blood pressure, renal function, marker for oxidative stress (OS), and CML in young WKY rats and SHR. We found blood pressure was increased in SHR with no difference in renal function and OS compared to WKY. CML was elevated in plasma (2.3 +/- 0.3 vs. 1.3 +/- 0.2 micromol/L) and kidney (1.0 +/- 0.1 vs. 0.5 +/- 0.1 micromol/L) compared to WKY. Early CML accumulation may contribute to the development of hypertension potentially by inducing early renal inflammation independent of glomerular dysfunction or oxidative stress.

摘要

晚期糖基化终末产物(AGEs)与高血压有关。与WKY大鼠相比,N-ε-(羧甲基)赖氨酸(CML)是否促成年轻自发性高血压大鼠(SHR)高血压的发生尚待确定。我们测定了年轻WKY大鼠和SHR的血压、肾功能、氧化应激(OS)标志物及CML。我们发现,与WKY大鼠相比,SHR的血压升高,而肾功能和OS无差异。与WKY大鼠相比,SHR血浆中CML升高(2.3±0.3对1.3±0.2微摩尔/升),肾脏中CML也升高(1.0±0.1对0.5±0.1微摩尔/升)。早期CML蓄积可能通过独立于肾小球功能障碍或氧化应激诱导早期肾脏炎症,从而促成高血压的发生。

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