The acute effect of angiotensin II on adrenal and anterior pituitary function in normal subjects and subjects with primary hyperaldosteronism.
Previous studies have shown that infused angiotensin II acutely suppresses ACTH release. In normal human subjects, the response to angiotensin II infused alone is specific to aldosterone and 18-hydroxycorticosterone. Other compounds such as cortisol, corticosterone and DOC do not respond. This is transformed into a general adrenocortical response by infusing small, constant quantities of ACTH. In patients with primary hyperaldosteronism, a poor response of plasma aldosterone to angiotensin II infused alone was altered to a response comparable with that in normal subjects by supplying ACTH during the infusion. Aldosterone secretion is more sensitive to ACTH in cases of primary hyperaldosteronism than in normal subjects. The poor response to angiotensin infusion may have been caused by inhibition of ACTH release, a phenomenon shown to occur in normal human subjects.
D000311:Adrenal Glands / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II; D001794:Blood Pressure; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology*; D008297:Male; D010903:Pituitary Gland, Anterior / Q000503:physiopathology*; D011188:Potassium / Q000097:blood
D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D011188:Potassium