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Aldosterone esters and the heart
C E Gomez-Sanchez1, M F Foecking, E P Gomez-Sanchez
1Division of Endocrinology, Montgomery VA Medical Center, The University of Mississippi Medical Center, Jackson 39216-4505, USA. cgomez-sanchez@medicine.umsmed.edu
American Journal of Hypertension
|June 20, 2001
Summary
Researchers identified a potent aldosterone derivative in rat hearts, potentially explaining mineralocorticoid excess symptoms despite low renin and aldosterone levels. This finding suggests localized regulation of mineralocorticoid activity in non-epithelial tissues.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Biochemistry
Background:
- Mineralocorticoid excess symptoms can occur despite low plasma renin and aldosterone.
- A potent, heart-derived mineralocorticoid factor was previously hypothesized.
- Aldosterone derivatives, like monoacetates, are rapidly hydrolyzed in circulation.
Purpose of the Study:
- To investigate the presence and nature of a potent mineralocorticoid in rat hearts.
- To determine if aldosterone derivatives could explain mineralocorticoid excess.
- To explore the regulation of aldosterone in non-epithelial tissues.
Main Methods:
- Extraction of rat hearts and plasma under conditions minimizing hydrolysis.
- Analysis using Thin-Layer Chromatography (TLC) and High-Performance Liquid Chromatography (HPLC).
- Comparison of extracted compounds with aldosterone monoacetate standards.
Main Results:
- 68% of extracted myocardial aldosterone corresponded to a derivative migrating like aldosterone-20-monoacetate.
- Tritiated aldosterone-21-monoacetate rapidly hydrolyzed to aldosterone in blood and heart tissue.
- The precise identity of the myocardial aldosterone derivative requires further confirmation.
Conclusions:
- A potent aldosterone derivative may be present in cardiac tissue.
- This derivative could be responsible for mineralocorticoid excess independent of systemic renin-aldosterone regulation.
- Local regulation of this derivative in non-epithelial tissues might bypass systemic hormonal control.