Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

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
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Increased expression of the mineralocorticoid receptor in the brain of spontaneously hypertensive rats.

Journal of neuroendocrinology·2012
Same author

Progress in primary aldosteronism: present challenges and perspectives.

Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme·2010
Same author

A highly sensitive immunofluorometric assay for the measurement of aldosterone in small sample volumes: validation in mouse serum.

The Journal of endocrinology·2008
Same author

11beta-hydroxylase and aldosterone synthase expression in fetal rat hippocampal neurons.

Journal of molecular endocrinology·2002
Same author

Editorial: Cardiac steroidogenesis--new sites of synthesis, or much ado about nothing?

The Journal of clinical endocrinology and metabolism·2001
Same author

The 11beta hydroxysteroid dehydrogenase 2 exists as an inactive dimer.

Steroids·2001

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).

Related Experiment Videos

  • 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.