Is the vascular endothelium under the control of aldosterone? Facts and hypothesis

Oberleithner, Hans

doi:10.1007/s00424-007-0205-7

Cited by 34 publications

(38 citation statements)

References 43 publications

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“…We were able to show that aldosterone dose-dependently increases endothelial cell volume and apical surface [18]. The effects were consistent in HUVEC, EAHy926, human coronary artery endothelial cells, and bovine aortic endothelial cells, i.e., in cells of both venous and arterial origin [18,33]. Importantly, opposite to the estradiol effects, with aldosterone cell surface, increased to a much larger extent than volume.…”

Section: Aldosteronesupporting

confidence: 51%

“…AFM is a nanotechnique that allows exact imaging of the surface of living cells [33,52]. Importantly, AFM is a scanning procedure that relies on a mechanical sensor with defined properties.…”

Section: Aldosteronementioning

confidence: 99%

“…From these measurements, the force necessary to indent a cell for a certain distance can be calculated. These forces relate directly to cell stiffness [33]. A schematic view of the development of force-distance curves is delineated in Fig.…”

Section: Aldosteronementioning

confidence: 99%

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How steroid hormones act on the endothelium—insights by atomic force microscopy

Hillebrand

Hausberg

Lang

et al. 2008

Pflugers Arch - Eur J Physiol

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Vascular actions of steroid hormones have gained increasing importance. Indeed, some steroid hormones favorably influence vascular structure and function, whereas others are detrimental. This review will focus on the endothelial effects of steroid hormones. In the first part, we summarize data from in vivo studies elucidating the regulation of endothelial function by steroid hormones. Accumulating data argue for an improvement of endothelium-derived relaxation and impaired vascular contraction by estradiol, whereas testosterone, progesterone, and aldosterone have contrary effects. In the second part, we present data from novel atomic force microscopy studies performed in living endothelial cells under the influence of steroid hormones. These studies provide insight into structural and functional alterations of endothelial cells characterized by changes in volume, apical surface, and stiffness. We summarize the available evidence that changes in shape of endothelial cells translate into changes of endothelial cell stiffness. Under the influence of estradiol, endothelial cells become spherical with consecutive improvement of elasticity, whereas aldosterone flattens endothelial cell-shape leading to increased stiffness. Both, endothelial cell shape and stiffness are major determinants of endothelial nitric oxide production. These studies emphasize the great potential of atomic force microscopy to investigate the function of living endothelial cells.Keywords Aldosterone . Glucocorticoids . Sex hormones . Atomic force microscopy . Endothelium . Imaging . Nitric oxideResearch over the last two decades has been clearly demonstrating that the vascular endothelium is a target for steroid hormones, e.g., sex hormones, glucocorticoids, and mineralocorticoids [25,35]. Indeed, specific receptors for these steroid hormones have been identified in endothelial cells. Numerous clinical studies demonstrate that the various steroid hormones affect vascular function in different ways. Sex hormonesVascular endothelial cells and vascular smooth muscle cells express receptors for estradiol, progesterone, and testosterone [54,55,66]. The sex hormones bind to specific cytosolic receptors. The resulting complexes are transported into the nucleus and initiate gene transcription (so-called genomic effects). Moreover, sex hormones cause a number of rapid non-genomic effects on vascular endothelial and smooth muscle cells.Several studies report gender differences in vascular function. Vascular contraction was found to be greater in male and ovarectomized female rats than in castrated male and female rats, suggesting an effect of testosterone in favor of vascular contraction and an effect of estradiol in favor of preventing vascular contraction [24]. Specifically, estradiol has been shown to cause endothelium-mediated vasorelaxation, whereas testosterone and progesterone interfere with estradiol-mediated endothelium-dependent vasodilation [25].There is a body of evidence suggesting that sex hormones interfere with the synthesis and b...

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Section: Aldosteronesupporting

confidence: 51%

Section: Aldosteronementioning

confidence: 99%

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How steroid hormones act on the endothelium—insights by atomic force microscopy

Hillebrand

Hausberg

Lang

et al. 2008

Pflugers Arch - Eur J Physiol

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“…Nevertheless, acute aldosterone application to endothelial cells also leads to amiloride-inhibitable cell swelling, which is most likely caused by the uptake of sodium and water (27). When endothelial cell pressure (technically indistinguishable of cell stiffness) is measured in response to the acute administration of aldosterone with the same time scale (Ϸ30 min), endothelial cells regulate their volume, while intracellular pressure increases (28). In addition, cells show signs of contraction.…”

Section: Role Of Epithelial Sodium Channels In Modulating Endothelialmentioning

confidence: 99%

Plasma sodium stiffens vascular endothelium and reduces nitric oxide release

Oberleithner

Riethmüller²,

Schillers³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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430

408

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“…Atomic force microscopy (AFM), however, allows high-resolution imaging under physiological conditions. This allows the study of functional changes in structure as shown, e.g., for nuclear pores [17,68,69,81,91] and endothelial cells [66,87].…”

Section: Introductionmentioning

confidence: 99%

Imaging CFTR in its native environment

Schillers¹

2007

Pflugers Arch - Eur J Physiol

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Application of atomic force microscopy (AFM) on isolated plasma membranes is a valuable method to study membrane proteins down to single-molecule level in their native environment. The cystic fibrosis transmembrane conductance regulator (CFTR), a protein of the adenosine triphosphate-binding cassette transporter superfamily, is known to play a crucial role in maintaining the salt and water balance on the epithelium and to influence processes such as cell volume regulation. A mutation in the gene encoding for CFTR results in cystic fibrosis (CF), a very common lethal genetic disease. Identification of CFTR within the cell membrane at the single-molecule level makes it feasible to visualize the distribution and organization of CFTR proteins within the cell membrane of healthy individuals and CF patients. We were able to show that human red blood cells have a CFTR distribution comparable to that of epithelial cells and that the number of CFTR in cells derived from CF patients is strongly reduced. Studies on CFTR-expressing oocytes disclose CFTR dynamics upon CFTR activation. We observed that cyclic adenosine monophosphate induces an insertion of CFTR in the plasma membrane and the formation of heteromeric CFTR-containing structures with yet unknown stoichiometry. The structure of CFTR was identified by highresolution scans of immunogold-labeled CFTR, revealing that CFTR forms a tail-to-tail dimer with a central pore. In conclusion, these studies show that AFM experiments on isolated plasma membranes allow not only quantification and localization of membrane proteins but also provide insight in their dynamics at a single-molecule level.

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Is the vascular endothelium under the control of aldosterone? Facts and hypothesis

Cited by 34 publications

References 43 publications

How steroid hormones act on the endothelium—insights by atomic force microscopy

How steroid hormones act on the endothelium—insights by atomic force microscopy

Plasma sodium stiffens vascular endothelium and reduces nitric oxide release

Imaging CFTR in its native environment

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