Detail of "379-68-0"

Reference

Effect of spironolactone on electrolytes, renin, ACTH and corticosteroids in the rat

Effect of spironolactone on electrolytes, renin, ACTH and corticosteroids in the rat. Chabert, P. R.; Guelpa-Decorzant, C.; Riondel, A. M.; Vallotton, M. B. (Dep. Med., Cantonal Univ. Hosp., Geneva, Switz.). J. Steroid Biochem., 20(6A), 1253-9 (English) 1984. CODEN: JSTBBK. ISSN: 0022-4731. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Spironolactone [52-01-7] (20-30 mg/kg/day) injected s.c. into rats on a normal Na+ diet slightly increased the urinary Na+/K+ ratio on the 1st day of treatment and markedly increased aldosterone [52-39-1], but not corticosterone [50-22-6], excretion, but did not affect fecal electrolyte excretion. It also caused a 6-fold increase in plasma aldosterone levels, a less marked rise in renin [9015-94-5] and progesterone [57-83-0], a delayed increase in DOC [64-85-7], and no change in ACTH [9002-60-2], 18-hydroxydeoxycorticosterone [379-68-0], or corticosterone concn. In animals maintained on a low Na+ diet, treatment increased urinary Na+/K+ ratio and aldosterone levels in urine and plasma; it did not change corticosterone values. In intact rats, the antimineralocorticoid action of spironolactone was characterized by an increase in Na+ excretion but no change in K+ elimination. No inhibitory effect of spironolactone on aldosterone, corticosterone, or 18-hydroxycorticosterone biosynthesis were demonstrated in this exptl. model.

Metabolism of exogenous steroids by rat adrenocortical cells in culture: significance of hydroxylation in the 11b or 18 position

Metabolism of exogenous steroids by rat adrenocortical cells in culture: significance of hydroxylation in the 11b or 18 position. Ramirez, Leyla C.; Maume, Bernard F. (Fac. Sci., Univ. Dijon, Dijon 21004, Fr.). C. R. Seances Soc. Biol. Ses Fil., 178(1), 77-83 (French) 1984. CODEN: CRSBAW. ISSN: 0037-9026. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 13 The role of 11b- and 18-hydroxylation in the biosynthesis and metab. of corticosteroids was investigated using newborn rat adrenocortical cell cultures and various exogenous substrates. The principal path for metab. of steroids was by formation of 18-hydroxydeoxycorticosterone [379-68-0] and corticosterone [50-22-6] via deoxycorticosterone [64-85-7]. The weak hydroxylation in position 21 of 11b- [600-57-7] and 18-hydroxyprogesterone [596-69-0] indicated that the route by these intermediates, while possible, is secondary. Apparently, 17-hydroxyprogesterone [68-96-2] and progesterone [57-83-0] are the principal substrates of 21-steroid hydroxylase whereas 11b-hydroxyprogesterone had a weak affinity for this enzyme. The 11b/18-hydroxylation of hydroxyprogesterone and hydroxydeoxycorticosterone derivs. was also examd.