Urine electrolyte response to 18-hydroxy-11-deoxycorticosterone in normal man.
1. To assess whether the adrenal corticosteroid 18-hydroxy-11-deoxycorticosterone [18-(OH)-DOC] affects urine electrolyte excretion in normal man, seven male volunteers received 120 microgram (353 nmol) intravenously in 1 h. This was compared with glucose (50 g/l; control) and aldosterone (80 microgram, 222 nmol) infusions in the same subjects. 2. A definite though weak antinatriuretic response to 18-(OH)DOC was observed, whereas urine potassium excretion was not altered. Aldosterone increased urine potassium excretion and reduced sodium output. Urine pH was lowered by both corticosteroids, aldosterone in general having a more marked effect. Urine volume was not altered by 18-(OH)DOC. 3. Plasma concentrations of 18-(OH)DOC and aldosterone rose approximately tenfold during their respective infusions. Compared with that of aldosterone, the metabolic clearance rate of 18-(OH)DOC was slower andits plasma half-life was longer. 4. We have been able to demonstrate that 18-(OH)DOC has a definite, albeit weak antinatriuretic action in normal man, but whether or not this corticosteroid is capable of elevating the blood pressure in man remains to be shown.
D015070:18-Hydroxydesoxycorticosterone / Q000097:blood / Q000494:pharmacology*; D000450:Aldosterone / Q000097:blood / Q000494:pharmacology; D003900:Desoxycorticosterone / Q000031:analogs & derivatives*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D011188:Potassium / Q000652:urine*; D012964:Sodium / Q000652:urine*
D015070:18-Hydroxydesoxycorticosterone; D003900:Desoxycorticosterone; D000450:Aldosterone; D012964:Sodium; D011188:Potassium