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Cited by 475

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Aldosterone: A Mediator of Myocardial Necrosis and Renal Arteriopathy

Rocha, R.·2000·Endocrinology

Abstract

To determine the role of aldosterone in mediating cardiovascular damage, we performed ablation/replacement experiments with aldosterone in a rat model of cardiac injury. Administration of angiotensin II and Nomega-nitro-L-arginine methyl ester (L-NAME; nitric oxide synthesis inhibitor) to male rats drinking 1% saline caused hypertension, severe biventricular myocardial necrosis, proteinuria, and fibrinoid necrosis of renal and cardiac vessels. Removal of aldosterone by adrenalectomy or through administration of the selective aldosterone antagonist eplerenone markedly reduced the cardiac and renal damage without significantly altering blood pressure. Aldosterone infusion in adrenalectomized, glucocorticoid-replaced L-NAME/angiotensin II-treated animals restored damage. Thus, we identified aldosterone as a critical mediator of L-NAME/angiotensin II induced vascular damage through mechanisms apparently independent of its effects on systolic blood pressure.

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Metadata

Authors
Rocha, R.
Venue
Endocrinology
Published
2000-10-01
Volume
141
Issue
10
Pages
3871-3878
ISSN
0013-7227 (ISSN-L)
OpenAlex
W2096645292
Cited by
475
References
3
FWCI
18.85
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Aldosterone: A Mediator of Myocardial Necrosis and Renal Arteriopathy. https://app.cochat.ai/papers/10.1210/en.141.10.3871
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Rocha, R. (2000). Aldosterone: A Mediator of Myocardial Necrosis and Renal Arteriopathy. Endocrinology. https://doi.org/10.1210/en.141.10.3871

Data sources

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.