Selective hypoaldosteronism: a study of steroid biosynthetic pathways under adrenocorticotrophin and angiotensin II infusion.
1. The functional integrity of the adrenal cortex has been tested in a case of selective hypoaldosteronism by adrenocorticotrophin (ACTH) and angiotensin II (AII) infusion. 2. During ACTH infusion a normal functioning zona fasciculata was indicated by the impressive increase of the ACTH-dependent plasma steroids; the aldosterone response was moderate. 3. During AII infusion the plasma aldosterone response was blunted with an unexpected dose-dependent increase in pregnenolone, resulting in abnormal decreasing progesterone/pregnenolone ratios during the infusion, suggesting a slow-down in the conversion of pregnenolone into progesterone. 4. This defect, a probable consequence of chronic renin deficiency on the zona glomerulosa, could be a contributing factor to the hypoaldosteronism.
D000302:Adrenal Cortex / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000450:Aldosterone / Q000172:deficiency*; D000804:Angiotensin II / Q000494:pharmacology; D005260:Female; D006801:Humans; D006889:Hydroxycorticosteroids / Q000097:blood; D008875:Middle Aged; D011372:Progestins / Q000097:blood; D013268:Stimulation, Chemical
D006889:Hydroxycorticosteroids; D011372:Progestins; D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone