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Journal of Renin-Angiotensin-Aldosterone System
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Rat model for investigating ACTH-independent angiotensin-induced aldosterone secretion

Darren M Roesch

Divisions of Endocrinology and Metabolism and Nephrology and Hypertension and Department of Medicine, Georgetown University, Washington, DC, USA, roeschd@gunet. georgetown.edu

Ying Tian

Divisions of Endocrinology and Metabolism and Nephrology and Hypertension and Department of Medicine, Georgetown University, Washington, DC, USA

Joseph G Verbalis

Divisions of Endocrinology and Metabolism and Nephrology and Hypertension and Department of Medicine, Georgetown University, Washington, DC, USA

Kathryn Sandberg

Divisions of Endocrinology and Metabolism and Nephrology and Hypertension and Department of Medicine, Georgetown University, Washington, DC, USA

Study of the acute effects of angiotensin II (Ang II) on aldosterone secretion has been hindered by the confounding influence of Ang II-induced adrenocorticotropic hormone (ACTH) secretion on aldosterone secretion, and by the fact that when laboratory rats are fed standard laboratory chows that are high in sodium, the adrenal is only minimally responsive to Ang II. In this study, we report the development of a model of Ang II-induced aldosterone secretion in NaCl-deprived, dexamethasone (DEX)-treated rats. This model allows the observation of (a) a high magnitude of Ang II-induced aldosterone secretion, (b) a return of plasma aldosterone levels to baseline after stimulation, and (c) aldosterone secretion without the potentially confounding influence of ACTH stimulation.

Key Words: aldosterone • angiotensin II • adrenocorticotropic hormone • dexamethasone • sodium deprivation

References

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Journal of Renin-Angiotensin-Aldosterone System, Vol. 1, No. 1, 36-39 (2000)
DOI: 10.3317/jraas.2000.008


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This Article
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Right arrow PubMed Citation
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Right arrow Articles by Sandberg, K.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*DEXAMETHASONE
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