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血浆钠会使血管内皮变硬并减少一氧化氮的释放。

Plasma sodium stiffens vascular endothelium and reduces nitric oxide release.

作者信息

Oberleithner Hans, Riethmüller Christoph, Schillers Hermann, MacGregor Graham A, de Wardener Hugh E, Hausberg Martin

机构信息

Institute of Physiology II and Department of Internal Medicine D, University of Münster, 48149 Münster, Germany.

出版信息

Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16281-6. doi: 10.1073/pnas.0707791104. Epub 2007 Oct 2.

DOI:10.1073/pnas.0707791104
PMID:17911245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1999397/
Abstract

Dietary salt plays a major role in the regulation of blood pressure, and the mineralocorticoid hormone aldosterone controls salt homeostasis and extracellular volume. Recent observations suggest that a small increase in plasma sodium concentration may contribute to the pressor response of dietary salt. Because endothelial cells are (i) sensitive to aldosterone, (ii) in physical contact with plasma sodium, and (iii) crucial regulators of vascular tone, we tested whether acute changes in plasma sodium concentration, within the physiological range, can alter the physical properties of endothelial cells. The tip of an atomic force microscope was used as a nanosensor to measure stiffness of living endothelial cells incubated for 3 days in a culture medium containing aldosterone at a physiological concentration (0.45 nM). Endothelial cell stiffness was unaffected by acute changes in sodium concentration <135 mM but rose steeply between 135 and 145 mM. The increase in stiffness occurred within minutes. Lack of aldosterone in the culture medium or treatment with the epithelial sodium channel inhibitor amiloride prevented this response. Nitric oxide formation was found down-regulated in cells cultured in aldosterone-containing high sodium medium. The results suggest that changes in plasma sodium concentration per se may affect endothelial function and thus control vascular tone.

摘要

膳食盐在血压调节中起主要作用,盐皮质激素醛固酮控制盐稳态和细胞外液量。最近的观察结果表明,血浆钠浓度的小幅升高可能导致膳食盐的升压反应。由于内皮细胞(i)对醛固酮敏感,(ii)与血浆钠有物理接触,且(iii)是血管张力的关键调节因子,我们测试了生理范围内血浆钠浓度的急性变化是否会改变内皮细胞的物理特性。原子力显微镜的尖端被用作纳米传感器,以测量在含有生理浓度(0.45 nM)醛固酮的培养基中培养3天的活内皮细胞的硬度。钠浓度<135 mM的急性变化对内皮细胞硬度没有影响,但在135至145 mM之间急剧上升。硬度增加在几分钟内发生。培养基中缺乏醛固酮或用上皮钠通道抑制剂氨氯地平处理可阻止这种反应。发现在含醛固酮的高钠培养基中培养的细胞中一氧化氮的生成被下调。结果表明,血浆钠浓度本身的变化可能影响内皮功能,从而控制血管张力。

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本文引用的文献

1
Is the vascular endothelium under the control of aldosterone? Facts and hypothesis.血管内皮受醛固酮的调控吗?事实与假说。
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