InChI key
VPGRYOFKCNULNK-ACXQXYJUSA-N
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
SMILES string
[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
assay
98%
form
solid
Gene Information
human ... NR3C2(4306)
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Riccardo Candido et al.
American journal of hypertension, 18(6), 844-850 (2005-06-01)
The aim of the present study was to compare glomerular permeability alterations associated with experimental hypertension models known to have different effects on the circulating renin-angiotensin system (RAS). Five groups, 10 animals each, were studied. One group served as a
J P Davis et al.
Clinical science (London, England : 1979), 81(1), 73-78 (1991-07-01)
1. Hypertension was induced in male Sprague-Dawley rats by left unilateral nephrectomy and deoxycorticosterone acetate--salt administration. After 5 weeks, arterial systolic blood pressure was significantly elevated in these animals (191.5 +/- 6.0 mmHg, mean +/- SD, n = 17) compared
Saad Lahlou et al.
Fundamental & clinical pharmacology, 17(3), 323-330 (2003-06-14)
The present study investigated the hypotensive responses to intravenous (i.v.) treatment with the essential oil of Alpinia zerumbet (EOAZ) and its main constituent, terpinen-4-ol (Trp-4-ol), in the experimental model of deoxycorticosterone-acetate (DOCA)-salt hypertensive rat. In both DOCA-salt hypertensive and uninephrectomized
Ibrahim F Benter et al.
Vascular pharmacology, 51(2-3), 101-109 (2009-05-05)
Renal dysfunction is a major cause of morbidity and mortality in patients with hypertension. In an attempt to understand the molecular mechanisms leading to renal dysfunction and in particular that of epidermal growth factor receptor (EGFR) and RasGTPase signaling, we
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
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