ASF acts as a true aldosterone secretagogue through mechanisms similar to Angiotensin II but via a distinct receptor site, which may be relevant to hypertension.
ASF identifies an angiotensin-independent aldosterone pathway in animals; hypothesis-generating and requires human validation before clinical consideration.
The steroidogenic properties of a glycoprotein fraction (ASF), isolated from normal human urine, were studied in cat adrenal capsular collagenase-dispersed cells and its effects compared to those of ACTH and Angiotensin II (AII). ACTH, AII and ASF induced dose-related increases in both aldosterone and cortisol production. In order of potency, ACTH = AII greater than ASF in stimulating aldosterone production and ACTH greater than AII greater than ASF in stimulating cortisol production. Increases in cAMP accompanied the steroidogenic response to ACTH but not to AII or ASF. The response to AII, but not to ASF, was inhibited (87% of normal) by equimolar concentrations of [Sar1, Thr8]AII, a specific AII antagonist. These results suggest that ASF is a true aldosterone secretagogue and that it initiates steroidogenesis by mechanisms similar to those of AII. However, the inability to block it effect with a specific antagonist of AII provides evidence for its action on a separate receptor site.
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Bravo et al. (1980) studied this question.
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