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  • Title: Stimulation and suppression of aldosterone in plasma of normal man and in primary aldosteronism.
    Author: Horton R.
    Journal: J Clin Invest; 1969 Jul; 48(7):1230-6. PubMed ID: 4307457.
    Abstract:
    The effect of stimulating and suppressive influences on plasma aldosterone in normal man and in patients with primary aldosteronism were studied using a sensitive double-isotope derivative assay for aldosterone. In normal sitting subjects, values were 9.2+/-0.9 (SE) mmug/100 ml and in subjects supine for 1 hr plasma aldosterone was 5.2+/-0.4 (SE) mmug/100 ml. Adrenocorticotropic hormone (ACTH), 0.5 U/hr, produced a rise of 46.8+/-22 (SE) mmug which was similar to the 1-hr effect of an infusion of a synthetic ACTH (beta(1-24), Cortrosyn). Angiotensin II in pressor amounts also increased plasma aldosterone 21.5+/-2.9 (SE) without change in plasma cortisol, whereas a subpressor dose ([unk]) had minimal effect.Fludrocortisone, 1.2 mg/day for 3 days, suppressed plasma aldosterone levels to 1.8+/-0.7 (SE) mmug/100 ml in five normal sitting subjects (P < 0.01); however, dexamethasone, 2 mg/day for 1-2 days, did not lower aldosterone concentration in plasma. In six patients with primary aldosteronism, plasma aldosterone on a normal sodium diet was 39.1+/-4.4 (SE) which differed significantly from normal sitting or supine subjects (P < 0.001). In contrast to the normal subjects, neither a pressor infusion of angiotensin II for 1 hr, nor fludrocortisone, 1.2 mg/day for 3 days, impressively altered plasma aldosterone levels. This approach appears to be useful for the study of the acute physiology and control mechanisms of aldosterone production in normal and hypertensive man.
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