The effect of dexamethasone on the control of plasma aldosterone concentration in normal recumbent man.
In order to evaluate the control of the circadian rhythm of plasma aldosterone concentration in man, plasma aldosterone, cortisol, sodium and potassium concentrations, and plasma renin activity (PRA) were measured in samples obtained at 20-minute intervals from 0200 to 0800 in sodium repleted (180 mEq. per day of diet) and sodium depleted (22 mEq. per day of diet) normal subjects. During sodium replete studies, plasma aldosterone and cortisol concentrations were significantly correlated (p greater than 0.01) in all 4 subjects. Plasma aldosterone also correlated with PRA (p greather than 0.01) in 2 subjects and with potassium (p greater than 0.01) in one. Episodic increases in plasma aldosterone concentration were observed despite suppression of ACTH by dexamethasone treatment. Plasma aldosterone concentrations were significantly correlated with PRA (p greater than 0.05 and p greater than 0.01) in only 2 of 4 subjects under these conditions. Following sodium restriction, plasma aldosterone concentrations were not significantly correlated with plasma cortisol and only infrequently with either PRA or potassium. When dexamethasone was administered during the low sodium diet, correlations with PRA (p greater than 0.001) were seen in 2 of 3 subjects and with potassium (p greater than 0.01) in 1 of 3 subjects. There was no significant correlation between plasma aldosterone and sodium concentration during any of the studies. These results are compatible with the concept that the relative importance of PRA, ACTH, and potassium in inducing changes in aldosterone production during the early morning hours is partially dependent upon dietary sodium, but also varies between individuals studied during similar sodium diets. The episodic alterations of plasma aldosterone concentration continued after ACTH was suppressed by dexamethasone pretreatment. These changes, in the absence of a consistent significant correlation with PRA and sodium and potassium concentrations, further suggest that another factor(s) may be important in controlling aldosterone production in recumbent normal subjects.
D000284:Administration, Oral; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000008:administration & dosage / Q000097:blood*; D002940:Circadian Rhythm / Q000187:drug effects*; D003907:Dexamethasone / Q000494:pharmacology*; D004039:Diet, Sodium-Restricted; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D011187:Posture; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood; D012890:Sleep; D012964:Sodium / Q000097:blood / Q000652:urine
D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D012083:Renin; D011188:Potassium; D006854:Hydrocortisone