Effect of a spirolactone on plasma and urinary aldosterone in primary aldosteronism.
In primary aldosteronism due to an adrenal adenoma (n=2), treatment with a spirolactone (160 mg Canrenone/day for 7 days) decreased plasma aldosterone and urinary aldosterone-18-glucuronide. However, in the presence of a normalization in urinary aldosterone 18-glucuronide plasma aldosterone remained elevated above normal. Continued therapy with higher doses (320 mg/day for 7 days and 480 mg/day for 28 days) did not significantly alter plasma aldosterone, while urinary aldosterone-18-glucuronide returned to values comparable to those obtained before therapy. Cessation of the drug resulted in a marked increase in plasma aldosterone and urinary aldosterone-18-glucuronide. The results indicate that in primary aldosteronism due to an adrenal adenoma, the spirolactone (Canrenone) inhibits aldosterone biosynthesis and seems to influence aldosterone degradation.
D000236:Adenoma / Q000150:complications / Q000378:metabolism; D000310:Adrenal Gland Neoplasms / Q000150:complications / Q000378:metabolism; D000450:Aldosterone / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002192:Canrenone; D005260:Female; D005965:Glucuronates / Q000652:urine; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology / Q000378:metabolism*; D007700:Kinetics; D011188:Potassium / Q000097:blood; D011245:Pregnadienes; D012083:Renin / Q000097:blood
D005965:Glucuronates; D011245:Pregnadienes; D000450:Aldosterone; D002192:Canrenone; D012083:Renin; D011188:Potassium