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,
TRACY McINTOSH,
BRIAN BERELOWITZ,
MARGO HUDSON,
ROBERT SALZMAN,
JO ANN E. MANSON and
JAMES C. MELBY
Section of Endocrinology and Metabolism, Evans Memorial Department of Clinical Resear Boston, Massachusetts 02118
Departments of Medicine and Surgery, University Hospital and Bston University School of Medicine Boston, Massachusetts02118
Address requests for reprints to: Dr. James C. Melby, Endocrinologyand Metabolism, University Hospital, 75 East Newton Street, Boston, Massachusettes 02118.
Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin- derived peptides, some of which have aldosterone- stimulating properties. The present study evaluated plasma β-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurementswere obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for β3-endorphin assay was preincubated with sepharose-bound anti-jS-lipotropin to remove j8-lipotropin that cross-reacted with theβ-endorpnin RIA. Mean ±SE plasma β-endorphin levels at 0800 h were elevated in IHA patients (47 ± 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 ± 9), essential hypertension (16 ± 1), and normal control (20 ± 2; P < 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either β- endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.
* This work was supported by Grants-in-Aid 1-R23-HL-31049, RR- 533-NIH, 5-PO-HL-18318, 5-RO1-AM-12027, 5-P32-HL-07224, and 1- T30-AM-21683 SCOR from the NIH.
Recipient of a New Investigator Research Award from the NIH (1-R23-HL-31049).
Received August 15, 1984.
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