QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online April 24, 2006
doi: 10.1242/10.1242/jcs.02886

This Article Figures Only Full Text Full Text (PDF) A correction has been published Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oberleithner, H. Articles by Schillers, H. Search for Related Content PubMed PubMed Citation Articles by Oberleithner, H. Articles by Schillers, H.

Differential action of steroid hormones on human endothelium

¹ Institute of Physiology II, University Münster, 48149 Münster, Germany
² Department of Internal Medicine D, University Münster, 48149 Münster, Germany
³ Institute of Zoophysiology, University Münster, 48149 Münster, Germany

^* Author for correspondence (e-mail: oberlei{at}uni-muenster.de)

Accepted 11 January 2006

The action of glucocorticoids on vascular permeability is well established. However, little is known about the action of mineralocorticoids on the structure and function of blood vessels. As endothelial cells are targets for both glucocorticoids and mineralocorticoids, we exposed human umbilical vein endothelial cells to both types of steroids. Aldosterone (mineralocorticoid) and dexamethasone (glucocorticoid) were applied for 3 days in culture before measurements of transendothelial ion and macromolecule permeability, apical cell surface and cell stiffness were taken. Transendothelial ion permeability was measured with electrical cell impedance sensing, macromolecule permeability with fluorescence-labeled dextran and apical cell membrane surface by three-dimensional AFM imaging. Cell stiffness was measured using the AFM scanning tip as a mechanical nanosensor. We found that aldosterone increased both apical cell surface and apical cell stiffness significantly, while transendothelial permeability remained unaffected. By contrast, dexamethasone significantly decreased ion and macromolecule permeability, while apical cell surface and cell stiffness did not change. Specific receptor antagonists for dexamethasone (RU486) and aldosterone (spironolactone) prevented the observed responses. We conclude that glucocorticoids strengthen cell-to-cell contacts (`peripheral action'), whereas mineralocorticoids enlarge and stiffen cells (`central action'). This could explain the dexamethasone-mediated retention of fluid in the vascular system, and endothelial dysfunction in states of hyperaldosteronism.

Key words: Atomic force microscopy, Mineralocorticoid, Endothelial permeability, Endothelial cell surface, Spironolactone, Cell stiffness, Epithelial sodium channel

This article has been cited by other articles:

				C. Riethmuller, H. Oberleithner, M. Wilhelmi, J. Franz, E. Schlatter, J. Klokkers, and B. Edemir Translocation of Aquaporin-Containing Vesicles to the Plasma Membrane Is Facilitated by Actomyosin Relaxation Biophys. J., January 15, 2008; 94(2): 671 - 678. [Abstract] [Full Text] [PDF]

				H. Oberleithner, C. Riethmuller, H. Schillers, G. A. MacGregor, H. E. de Wardener, and M. Hausberg Plasma sodium stiffens vascular endothelium and reduces nitric oxide release PNAS, October 9, 2007; 104(41): 16281 - 16286. [Abstract] [Full Text] [PDF]