The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension
Open accessAbstract
Hypertension is a side effect of systemically administered glucocorticoids, but the underlying molecular mechanism remains poorly understood. Ingestion of dexamethasone by rats telemetrically instrumented increased blood pressure progressively over 7 days. Plasma concentrations of Na + and K + and urinary Na + and K + excretion remained constant, excluding a mineralocorticoid-mediated mechanism. Plasma NO 2 − /NO 3 − (the oxidation products of NO) decreased to 40%, and the expression of endothelial NO synthase (NOS III) was found down-regulated in the aorta and several other tissues of glucocorticoid-treated rats. The vasodilator response of resistance arterioles was tested by intravital microscopy in the mouse dorsal skinfold chamber model. Dexamethasone treatment significantly attenuated the relaxation to the endothelium-dependent vasodilator acetylcholine, but not to the endothelium-independent vasodilator S-nitroso- N -acetyl- d , l -penicillamine. Incubation of human umbilical vein endothelial cells, EA.hy 926 cells, or bovine aortic endothelial cells with several glucocorticoids reduced NOS III mRNA and protein expression to 60–70% of control, an effect that was prevented by the glucocorticoid receptor antagonist mifepristone. Glucocorticoids decreased NOS III mRNA stability and reduced the activity of the human NOS III promoter (3.5 kilobases) to ≈70% by decreasing the binding activity of the essential transcription factor GATA. The expressional down-regulation of endothelial NOS III may contribute to the hypertension caused by glucocorticoids.
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Cited by
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Endothelial glucocorticoid receptor is required for protection against sepsis
Goodwin, J. E., Feng, Y., Velazquez, H., & Sessa, W. C. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1210200110 · Cited by 142
Metadata
- Authors
- Wallerath, T., Witte, K., Schäfer, S. C., Schwarz, P. M., Prellwitz, W., Wohlfart, P., Kleinert, H., Lehr, H.-A., Lemmer, B., & Förstermann, U.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-11-09
- Volume
- 96
- Issue
- 23
- Pages
- 13357-13362
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2003465691
- Cited by
- 289
- References
- 30
- FWCI
- 4.67
- Type
- journal article
- Language
- en
- Open access
- green
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- Wallerath, T., Witte, K., Schäfer, S. C., Schwarz, P. M., Prellwitz, W., Wohlfart, P., Kleinert, H., Lehr, H.-A., Lemmer, B., & Förstermann, U. (1999). Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.23.13357
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
