SMILES字符串
C[C@]12CC[C@H]3[C@@H](CCC4=CC(=O)CC[C@]34CO)[C@@H]1CCC2=O
InChI
1S/C19H26O3/c1-18-8-7-16-14(15(18)4-5-17(18)22)3-2-12-10-13(21)6-9-19(12,16)11-20/h10,14-16,20H,2-9,11H2,1H3/t14-,15-,16-,18-,19+/m0/s1
InChI key
XGUHPTGEXRHMQQ-BGJMDTOESA-N
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H Sekihara et al.
Clinical endocrinology, 39(5), 557-560 (1993-11-01)
We have reported that 19-hydroxyandrostenedione (19-OH-A-dione) functions as an amplifier of the sodium-retaining and hypertensive action of aldosterone. We therefore measured 19-hydroxyandrostenedione in hypertensive patients. We studied 53 normal male control subjects and 63 male patients with essential hypertension (48
M Minato et al.
Nihon Naibunpi Gakkai zasshi, 66(1), 29-41 (1990-01-20)
In order to evaluate the hypertensinogenic action of 19-hydroxyandrostenedione (19-OH-AD), which has been reported to be an amplifier of mineralocorticoid, the changes in several humoral factors were observed in 19-OH-AD treated rats as compared to those in DOCA hypertensive rats.
K Higuchi et al.
Endocrinologia japonica, 36(6), 881-885 (1989-12-01)
The steroid, 19-hydroxyandrost-4-ene-3, 17-dione (19-hydroxyandrostene-dione, 19-OH-A-dione) has been known to enhance the mineralocorticoid action of aldosterone. To investigate the age-related change in the plasma 19-OH-A-dione concentration, plasma 19-OH-A-dione, androst-4-ene-3, 17-dione (A-dione), aldosterone and cortisol of 38 non-hypertensive healthy subjects (18
J P Weniger et al.
Journal of steroid biochemistry, 35(3-4), 507-510 (1990-03-01)
Ovaries from 18-21-day-old foetal as well as from 2-10-day-old infantile rats were cultured in vitro in the presence of [3H]19-hydroxyandrostenedione and in the presence or absence of LH, FSH or (Bu)2 cAMP, and oestrone and oestradiol formed were determined by
H Morita et al.
Endocrine journal, 40(1), 89-97 (1993-02-01)
The present study was performed to clarify changes in plasma levels of 19-hydroxyandrostenedione (19-OH-AD), an amplifier of aldosterone and a possible hypertensinogenic steroid, during several tests for the renin-angiotensin system in 20 patients with aldosterone-producing adenoma (APA) and to determine
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