Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:In vitro steroidogenic properties of a new hypertension-producing compound isolated from normal human urine. 624 62

The steroidogenic properties of a glycoprotein fraction (urinary ASF), isolated from normal human urine, were studied in collagenase-dispersed rabbit adrenal capsular cells in 1) define the requirements for its steroidogenic activity, and 2) assess its site and mode of action. When incubated with adrenal cell suspension at 37 degrees C for 2 hours, urinary ASF induced dose-related increases in both aldosterone and corticosterone production. However, urinary ASF was less potent (ED50 = 10(-9) M) than either angiotensin II (ED50 = 8 x 10(-11) M) or ACTH (ED50 = 4 x 10(-11) M). Increases in cyclic AMP accompanized the steroidogenic response to ACTH but not to either urinary ASF or AII. Deprivation of potassium in incubation media or the addition of ouabain (1 mM) during incubation completely inhibited the steroidogenic response to either urinary ASF, ACTH, or AII. Like ACTH and AII, urinary ASF increased conversion of corticosterone to aldosterone. Specific competitive antagonist of AII (Sar1, Thr8, AII) and ACTH ([I1e9]ACTH1-24) did not prevent the ASF-induced increase in aldosterone production. These results suggest that urinary ASF is readily distinguishable from ACTH. Although it shares similar steroidogenic properties with AII, the inability of AII antagonist to block its effects suggests that it acts at a separate receptor site.
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PMID:Steroidogenic characteristics of a new aldosterone-stimulating factor (ASF) isolated from normal human urine. 626 51