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方案
98%
表单
solid
SMILES字符串
[H][C@@]12CCC3=CC(=O)CC[C@]3(C)[C@@]1([H])CC[C@]4(C)[C@]([H])(CC[C@@]24[H])C(=O)COC(C)=O
InChI
1S/C23H32O4/c1-14(24)27-13-21(26)20-7-6-18-17-5-4-15-12-16(25)8-10-22(15,2)19(17)9-11-23(18,20)3/h12,17-20H,4-11,13H2,1-3H3/t17-,18-,19-,20+,22-,23-/m0/s1
InChI key
VPGRYOFKCNULNK-ACXQXYJUSA-N
基因信息
human ... NR3C2(4306)
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Z B Fortes et al.
Journal of hypertension, 8(11), 1043-1048 (1990-11-01)
In order to investigate if endothelium-derived contracting factor (EDCF) is involved in the altered reactivity of microvessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats, mesenteric arterioles, either perfused in vitro or studied in vivo in situ, were used. The responses to
Joseph Fomusi Ndisang et al.
The Journal of pharmacology and experimental therapeutics, 334(1), 87-98 (2010-04-16)
We investigated the role of heme oxygenase (HO), adiponectin, and atrial natriuretic peptide (ANP) in uninephrectomized (UnX) deoxycorticosterone-acetate (DOCA)-salt hypertensive rats, a volume-overload model characterized by elevated endothelin-1 (ET-1), mineralocorticoid-induced oxidative/inflammatory insults, fibrosis, hypertrophy, and severe renal histopathological lesions that
Volker Vallon et al.
Journal of molecular medicine (Berlin, Germany), 84(5), 396-404 (2006-04-11)
The mineralocorticoids aldosterone and deoxycorticosterone acetate (DOCA) stimulate renal tubular salt reabsorption, increase salt appetite, induce extracellular volume expansion, and elevate blood pressure. Cardiac effects of mineralocorticoids include stimulation of matrix protein deposition leading to cardiac fibrosis, which is at
D H Vandorpe et al.
Canadian journal of physiology and pharmacology, 69(11), 1784-1788 (1991-11-01)
Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary
Jiang Xu et al.
American journal of physiology. Heart and circulatory physiology, 299(5), H1328-H1338 (2010-09-14)
Angiotensin II (ANG II) contributes to hypertension, cardiac hypertrophy, fibrosis, and dysfunction; however, it is difficult to separate the cardiac effect of ANG II from its hemodynamic action in vivo. To overcome the limitations, we used transgenic mice with cardiac-specific
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