The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Glucocorticoids Activate Cardiac Mineralocorticoid Receptors During Experimental Myocardial Infarction
Open accessAbstract
Myocardial ischemia-reperfusion leads to significant changes in redox state, decreased postischemic functional recovery, and cardiomyocyte apoptosis, with development and progression of heart failure. Ischemia-reperfusion in the isolated perfused rat heart has been used as a model of heart failure. Clinically, mineralocorticoid receptor blockade in heart failure decreases morbidity and mortality versus standard care alone. The effects of corticosteroids on infarct area and apoptosis were determined in rat hearts subjected to 30 minutes of ischemia and 2.5 hours of reperfusion. Both aldosterone and cortisol increased infarct area and apoptotic index, an effect half-maximal between 1 and 10 nM and reversed by spironolactone. Dexamethasone and mifepristone aggravated infarct area and apoptotic index, similarly reversed by spironolactone. Spironolactone alone reduced infarct area and apoptotic index below ischemia-reperfusion alone, in hearts from both intact and adrenalectomized rats. The present study shows that cardiac damage is aggravated by activation of mineralocorticoid receptors by aldosterone or cortisol or of glucocorticoid receptors by dexamethasone. Mifepristone unexpectedly acted as a glucocorticoid receptor agonist, for which there are several precedents. Spironolactone protected cardiomyocytes via inverse agonist activity at mineralocorticoid receptors, an effect near maximal at a relatively low dose (10 nM). Spironolactone acts not merely by excluding corticosteroids from mineralocorticoid receptors but as a protective inverse agonist at low concentration. Mineralocorticoid receptor antagonists may, thus, provide an additional therapeutic advantage in unstable angina and acute myocardial infarction.
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Citations
Cites
1 retracted
Aldosterone Directly Induces Myocyte Apoptosis Through Calcineurin-Dependent Pathways
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RetractedThe Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure
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Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated
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Self-citationEvidence for an increased rate of cardiovascular events in patients with primary aldosteronism
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Regulation of Corepressor Function by Nuclear NADH
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Self-citation
Cited by
11β-hydroxysteroid dehydrogenases: Intracellular gate-keepers of tissue glucocorticoid action
Chapman, K., Holmes, M., & Seckl, J. (2013) · Physiological Reviews · doi:10.1152/physrev.00020.2012 · Cited by 887
Contribution of aldosterone to cardiovascular and renal inflammation and fibrosis
Brown, N. J. (2013) · Nature Reviews Nephrology · doi:10.1038/nrneph.2013.110 · Cited by 451
Di Dalmazi, G., Vicennati, V., Garelli, S., Casadio, E., Rinaldi, E., Giampalma, E., Mosconi, C., Golfieri, R., Paccapelo, A., Pagotto, U., et al. (2014) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(13)70211-0 · Cited by 415
Usher, M. G., Duan, S. Z., Ivaschenko, C. Y., Frieler, R. A., Berger, S., Schütz, G., Lumeng, C. N., & Mortensen, R. M. (2010) · Journal of Clinical Investigation · doi:10.1172/jci41080 · Cited by 383
Mechanism of Salt-Sensitive Hypertension: Focus on Adrenal and Sympathetic Nervous Systems
Fujita, T. (2014) · Journal of the American Society of Nephrology · doi:10.1681/asn.2013121258 · Cited by 124
Metadata
- Authors
- Mihailidou, A. S., Loan Le, T. Y., Mardini, M., & Funder, J. W.
- Venue
- Hypertension
- Published
- 2009-12
- Volume
- 54
- Issue
- 6
- Pages
- 1306-1312
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2129911320
- Cited by
- 262
- References
- 42
- FWCI
- 14.35
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Mihailidou, A. S., Loan Le, T. Y., Mardini, M., & Funder, J. W. (2009). Glucocorticoids Activate Cardiac Mineralocorticoid Receptors During Experimental Myocardial Infarction. Hypertension. https://doi.org/10.1161/hypertensionaha.109.136242
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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.
