Affiliation:
1. G.V. (Sonny) Montgomery VA Medical Center and Department of
Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson,
MS, United States of America
Abstract
AbstractThe initial isolation of adrenal steroids from large quantities of animal
adrenals resulted in an amorphous fraction resistant to crystallization and
identification and had potent effects on electrolyte transport. Aldosterone was
eventually isolated and identified in the fraction and was soon shown to cause
hypertension when in excess. The autonomous and excessive production of
aldosterone, primary aldosteronism, is the most common cause of secondary
hypertension. Aldosterone is metabolized in the liver and kidney, and its
metabolites are conjugated with glucuronic acid for excretion. The most common
liver metabolite is 3α,5β-tetrahydroaldosterone-3-glucuronide,
while that of the kidney is aldosterone-18-oxo-glucuronide. In terms of their
value, especially the aldosterone-18-oxo-glucuronide, is commonly used for the
diagnosis of primary aldosteronism because they provide an integrated value of
the total daily production of aldosterone. Conversion of aldosterone to
18-oxo-glucuronide is impeded by drugs, like some common non-steroidal
anti-inflammatory drugs that compete for UDP-glucuronosyltransferase-2B7, the
most important glucuronosyltransferase for aldosterone metabolism.
Tetrahydroaldosterone is the most abundant metabolite and the most reliable for
the diagnosis of primary aldosteronism, but it is not commonly measured.
Funder
National Heart, Lung, and Blood Institute
Subject
Endocrinology,General Medicine,Endocrinology, Diabetes and Metabolism,Internal Medicine