11-Dehydrocorticosterone is an endogenous mineralocorticoid.[1],[2],[3] It increases Na+/K+-ATPase mRNA expression in vascular smooth muscle cells and inhibits aldosterone action in B. marinus toad bladder tissue in a concentration-dependent manner.[1],[2] 11-Dehydrocorticosterone decreases the sodium/creatine ratio and increases the potassium/creatine ratio in rat urine in a dose-dependent manner in a model of 11β-hydroxysteroid dehydrogenase inhibition induced by carbenoxolone .[3] Chronic administration 11-dehydrocorticosterone increases plasma glucocorticoids levels, body weight gain, and adiposity, as well as induces insulin resistance in mice.[4]
Reference:
[1].Muto, S., Nemoto, J., Ebata, S., et al.Corticosterone and 11-dehydrocorticosterone stimulate Na,K-ATPase gene expression in vascular smooth muscle cellsKidney Int.54(2)492-508(1998)
[2].Brem, A.S., Matheson, K.L., Barnes, J.L., et al.11-Dehydrocorticosterone, a glucocorticoid metabolite, inhibits aldosterone action in toad bladderAm. J. Physiol.261(5)F873-F879(1991)
[3].Souness, G.W., and Morris, D.J.11-Dehydrocorticosterone in the presence of carbenoxolone is a more potent sodium retainer than corticosteroneSteroids58(1)24-28(1993)
[4].Harno, E., Cottrell, E.C., Keevil, B.G., et al.11-Dehydrocorticosterone causes metabolic syndrome, which is prevented when 11β-HSD1 is knocked out in livers of male miceEndocrinology154(10)3599-3609(2013)