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原发性高血压患者血浆内皮素-1和大内皮素-1水平

Circulating Levels of Endothelin-1 and Big Endothelin-1 in Patients with Essential Hypertension.

作者信息

Kostov Krasimir, Blazhev Alexander

机构信息

Department of Pathophysiology, Medical University-Pleven, 1 Kliment Ohridski Str., 5800 Pleven, Bulgaria.

Department of Biology, Medical University-Pleven, 1 Kliment Ohridski Str., 5800 Pleven, Bulgaria.

出版信息

Pathophysiology. 2021 Oct 25;28(4):489-495. doi: 10.3390/pathophysiology28040031.

DOI:10.3390/pathophysiology28040031
PMID:35366246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8830463/
Abstract

The role of endothelin-1 (ET-1) in the pathogenesis of hypertension (HTN) is not clearly established. There is evidence that its circulating levels are elevated in some forms of experimental and human HTN, but this was not a consistent finding. Based on these controversial data, we tested serum levels of ET-1 and Big ET-1 (the precursor of ET-1) in patients with essential HTN, comparing the results with those of healthy normotensive controls. The levels of ET-1 and Big ET-1 were measured by ELISA. Our results in patients with essential HTN showed that the mean levels of ET-1 (5.01 ± 2.1 pg/mL) were significantly higher ( = 6.34, = 0.0144) than the mean levels in the control group (3.2 ± 1.0 pg/mL). The levels of Big ET-1 in patients with essential HTN (0.377 ± 0.1 pmol/L) were similar to those in the control group (0.378 ± 0.07 pmol/L) and did not differ significantly ( = 0.00, = 0.9531). These data suggest that ET-1, but not Big ET-1, may play an important role in the pathogenesis of primary HTN.

摘要

内皮素-1(ET-1)在高血压(HTN)发病机制中的作用尚未明确确立。有证据表明,在某些形式的实验性高血压和人类高血压中,其循环水平会升高,但这并非是一个一致的发现。基于这些有争议的数据,我们检测了原发性高血压患者血清中ET-1和大ET-1(ET-1的前体)的水平,并将结果与健康血压正常的对照组进行比较。ET-1和大ET-1的水平通过酶联免疫吸附测定法(ELISA)进行测量。我们对原发性高血压患者的研究结果显示,ET-1的平均水平(5.01±2.1皮克/毫升)显著高于对照组的平均水平(3.2±1.0皮克/毫升)(t = 6.34,P = 0.0144)。原发性高血压患者中大ET-1的水平(0.377±0.1皮摩尔/升)与对照组(0.378±0.07皮摩尔/升)相似,且无显著差异(t = 0.00,P = 0.9531)。这些数据表明,ET-1而非大ET-1可能在原发性高血压的发病机制中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4698/8830463/9544828d7725/pathophysiology-28-00031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4698/8830463/64b12132fcf8/pathophysiology-28-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4698/8830463/9544828d7725/pathophysiology-28-00031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4698/8830463/64b12132fcf8/pathophysiology-28-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4698/8830463/9544828d7725/pathophysiology-28-00031-g002.jpg

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