Effect of naloxone on the adrenal cortex in primary aldosteronism.
Endogenous opioids have been suggested to play a pathogenetic role in idiopathic hyperaldosteronism (IHA). To investigate this issue, the opiate antagonist naloxone was administered to 8 normals and 14 patients with primary aldosteronism, 6 with an aldosterone-producing adenoma (APA) and 8 with IHA. In normals, APA, and IHA, naloxone caused a significant increase in plasma cortisol and no change in ACTH, renin activity (PRA), and aldosterone levels. All subjects were retested after dexamethasone 2 mg. ACTH and cortisol were reduced and PRA was unchanged without modifications after naloxone. Baseline aldosterone was unaltered in all. While normals and APA failed to show any aldosterone response to naloxone under dexamethasone, IHA patients demonstrated a significant decrease. beta-Endorphin concentrations were in the normal range before and after dexamethasone. In normals as well as in APA and IHA, naloxone may act directly on the adrenal cortex increasing zona fasciculata responsiveness to physiological levels of ACTH. The decrease of aldosterone induced by naloxone in IHA under dexamethasone may be due to an intra-adrenal opioid control of zona glomerulosa in this disorder.
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Institute of Semeiotica Medica, University of Padova, Italy.
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D000236:Adenoma / Q000503:physiopathology; D000302:Adrenal Cortex / Q000187:drug effects*; D000310:Adrenal Gland Neoplasms / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000450:Aldosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006929:Hyperaldosteronism / Q000097:blood / Q000503:physiopathology*; D009270:Naloxone / Q000494:pharmacology*; D012083:Renin / Q000097:blood
D009270:Naloxone; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D012083:Renin; D006854:Hydrocortisone