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Chemical Compound Review

Desocort     [2-(10,13-dimethyl-3-oxo- 1,2,6,7,8,9,11,12...

Synonyms: Descotone, Decsterone, Doca acetate, NSC-9567, SureCN1021137, ...
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Disease relevance of Decortin

  • (f) In rats depleted of potassium by low potassium intake or by production of DOCA hypertension, an inhibition of skeletal muscle Na+, K(+)-ATPase ion pump activity is directed by hypothalamic centers and involves inhibition by alpha-adrenergic activity of slow twitch fibers and inhibition by undetermined humoral factors of fast twitch fibers [1].
  • After an acid load in the absence of Na+ and HCO3-, pHi response to basolateral Na+ addition was stimulated (+66%) by acidosis, but not by DOCA [2].
  • When 10-15 mg i.m. of desoxycorticosterone acetate (DOCA) was given daily, five dogs developed sodium retention and ascites, while four escaped from DOCA [3].
  • A differential increase in ventricular weight to body weight (hypertrophy) occurred at 3 weeks in the SHR and aortic constriction models and at 4 weeks in the DOCA salt model [4].
  • The ET(A) antagonist prevented cardiac fibrosis in DOCA-salt rats [5].

Psychiatry related information on Decortin


High impact information on Decortin


Chemical compound and disease context of Decortin


Biological context of Decortin

  • In all four dogs who escaped from DOCA, the PCA was widely patent and the mean pressure gradient was only 1.6 cm H2O [3].
  • Isolated renal cortical collecting tubules obtained from rabbits treated chronically with desoxycorticosterone acetate (DOCA) have been found to possess elevated transepithelial potential differences and a greatly increased capacity for ion transport [16].
  • However, in DOCA-salt kidneys, BQ-3020 caused renal vasoconstriction (RPP, +5.4 +/- 2.4%, P < .01 versus control) and a much smaller NO release (+1.1 +/- 0.4 fmol.min-1.g-1 kidney wt, P < .01 versus control) [17].
  • Natriuresis of DOCA rats was significantly greater than that of either normal or responding NaD rats [18].
  • To investigate the possible contributions of cardiac volume overload and cardiac sympathetic hyperactivity in the effects of sodium on cardiac mass, we evaluated the effects of treatment with saline (1%) and deoxycorticosterone acetate + saline (DOCA/saline) for 10 days and 3 and 6 weeks on ventricular anatomy and intracardiac pressures [19].

Anatomical context of Decortin

  • Methylprednisolone and DOCA increased electrolyte and water transport and Na-K-ATPase activity concomitantly in specific segments of small intestine and colon [20].
  • In the kidney, anterior pituitary, testis, and choroid plexus of the brain, ACE levels correlated negatively with PRA, with lowest ACE levels in the 2K-1C group and highest levels in the DOCA-salt group [10].
  • Structural exmination of tubules from rabbits exposed to either DOCA or dexamethasone for 11--18 d reveals a marked increase in basolateral cell membrane area in these tubules [16].
  • In DOCA-salt rats, interstitial and perivascular collagen density was increased in the subendocardial and midmyocardial regions of the left ventricle (3- to 4-fold, P:<0.05), whereas in subepicardial myocardium, the increase was predominantly perivascular [5].
  • METHODS AND RESULTS: Rats were made hypertensive after one renal artery was clipped (two kidney, one-clip renal model) or after the administration of deoxycorticosterone and salt (DOCA-salt model) [21].

Associations of Decortin with other chemical compounds

  • Cilazapril had a marked preventive effect on neointima formation in normotensive rats, spontaneously hypertensive rats, and two-kidney, one-clip rats but was ineffective in DOCA rats [22].
  • To investigate possible relationships between mineralocorticoids, the renal kallikreinkinin system, and renal prostaglandins, we studied the effects of aldosterone and deoxycorticosterone acetate (DOCA) and of an inhibitor of kallikrein, aprotinin, on the urinary excretion of kallikrein and prostaglandin E-like substance (PGE) by the conscious rat [23].
  • Similarly, injections of DOCA (5 mg/day) into 14 rats increased the excretion of PGE and kallikrein, measured before and after 10 days of treatment, from 41.6 +/- 3.9 ng/day and 39.4 +/-4.9 U/day to 194.3 +/- 20.7 ng/day (P less than 0.001) and 90.6 +/- 14.7 U/day (P less than 0.001), respectively [23].
  • Captopril, candesartan, and spironolactone reversed the increased deposition of perivascular and interstitial collagen in DOCA-salt rats; the increased cardiac fibronectin deposition was reversed by candesartan and spironolactone [24].
  • Activation of NF-kappa-B and expression of I-kappa-B-alpha in DOCA-salt rats were normalized by fenofibrate [25].

Gene context of Decortin


Analytical, diagnostic and therapeutic context of Decortin

  • Plasma renin activity (PRA) was highest in the 2K-1C group (6.20 +/- 2.17 ng/ml per h), intermediate in the 1K-1C group (2.19 +/- 0.62 ng/ml per h) and control group (3.20 +/- 0.53 ng/ml per h), and lowest in the DOCA-salt group (0.07 +/- 0.06 ng/ml per h) [10].
  • Adrenalectomy had no influence on the tumor growth in PI-bearing animals, but DCA injections stimulated secretion production by both tumor cells and normal mammary cells [31].
  • Maximum induction was 10-fold over control at 5 weeks in the aortic constriction model, 8-fold at 3 weeks in the SHR, and 6-fold at 6 weeks in the DOCA salt model [4].
  • Northern blot analysis revealed that renal ETB mRNA was significantly decreased in DOCA-salt rat kidneys compared with controls (0.36 +/- 0.13 versus 1.00 +/- 0.23, P < .05) [17].
  • Normal sodium intake, local denervation, and peripheral sympathectomy had no effect on the development of these vascular changes in DOCA-treated rats [32].


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  3. Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites. Unikowsky, B., Wexler, M.J., Levy, M. J. Clin. Invest. (1983) [Pubmed]
  4. Induction of myocardial insulin-like growth factor-I gene expression in left ventricular hypertrophy. Donohue, T.J., Dworkin, L.D., Lango, M.N., Fliegner, K., Lango, R.P., Benstein, J.A., Slater, W.R., Catanese, V.M. Circulation (1994) [Pubmed]
  5. Myocardial fibrosis in DOCA-salt hypertensive rats: effect of endothelin ET(A) receptor antagonism. Ammarguellat, F., Larouche, I., Schiffrin, E.L. Circulation (2001) [Pubmed]
  6. The effects of deoxycorticosterone-induced sodium appetite on hedonic behaviors in the rat. Morris, M.J., Na, E.S., Grippo, A.J., Johnson, A.K. Behav. Neurosci. (2006) [Pubmed]
  7. Dietary suppression of prostaglandin synthesis does not accelerate DOCA/salt hypertension in rats. Codde, J.P., Croft, K.D., Beilin, L.J. Clin. Exp. Pharmacol. Physiol. (1987) [Pubmed]
  8. Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. Landmesser, U., Dikalov, S., Price, S.R., McCann, L., Fukai, T., Holland, S.M., Mitch, W.E., Harrison, D.G. J. Clin. Invest. (2003) [Pubmed]
  9. Chronic blockade of endogenous atrial natriuretic polypeptide (ANP) by monoclonal antibody against ANP accelerates the development of hypertension in spontaneously hypertensive and deoxycorticosterone acetate-salt-hypertensive rats. Itoh, H., Nakao, K., Mukoyama, M., Yamada, T., Hosoda, K., Shirakami, G., Morii, N., Sugawara, A., Saito, Y., Shiono, S. J. Clin. Invest. (1989) [Pubmed]
  10. Angiotensin-converting enzyme labeled with [3H]captopril. Tissue localizations and changes in different models of hypertension in the rat. Wilson, S.K., Lynch, D.R., Snyder, S.H. J. Clin. Invest. (1987) [Pubmed]
  11. Cardiovascular regulation by central adrenergic mechanisms and its alteration by hypotensive drugs. Haeusler, G. Circ. Res. (1975) [Pubmed]
  12. Vasopressin-central nervous system interactions in the development of DOCA hypertension. Berecek, K.H., Barron, K.W., Webb, R.L., Brody, M.J. Hypertension (1982) [Pubmed]
  13. Sensitivity of caudal arteries and the mesenteric vascular bed to norepinephrine in DOCA-salt hypertension. Longhurst, P.A., Rice, P.J., Taylor, D.A., Fleming, W.W. Hypertension (1988) [Pubmed]
  14. Kinin-mediated antihypertensive effect of captopril in deoxycorticosterone acetate-salt hypertension. Chen, K., Zhang, X., Dunham, E.W., Zimmerman, B.G. Hypertension (1996) [Pubmed]
  15. Relationship of vascular sodium-potassium pump activity to intracellular sodium in hypertensive rats. Brock, T.A., Smith, J.B., Overbeck, H.W. Hypertension (1982) [Pubmed]
  16. Modulation of cell membrane area in renal collecting tubules by corticosteroid hormones. Wade, J.B., O'Neil, R.G., Pryor, J.L., Boulpaep, E.L. J. Cell Biol. (1979) [Pubmed]
  17. Direct measurements of endothelium-derived nitric oxide release by stimulation of endothelin receptors in rat kidney and its alteration in salt-induced hypertension. Hirata, Y., Hayakawa, H., Suzuki, E., Kimura, K., Kikuchi, K., Nagano, T., Hirobe, M., Omata, M. Circulation (1995) [Pubmed]
  18. Collecting duct function in deoxycorticosterone acetate-escaped, normal, and salt-deprived rats. Response to hypervolemia. Sonnenberg, H. Circ. Res. (1976) [Pubmed]
  19. Sodium-induced cardiac hypertrophy. Cardiac sympathetic activity versus volume load. Fields, N.G., Yuan, B.X., Leenen, F.H. Circ. Res. (1991) [Pubmed]
  20. Na+-K+-activated adenosine triphosphatase and intestinal electrolyte transport. Effect of adrenal steroids. Charney, A.N., Kinsey, M.D., Myers, L., Gainnella, R.A., Gots, R.E. J. Clin. Invest. (1975) [Pubmed]
  21. Hypertension increases connexin43 in a tissue-specific manner. Haefliger, J.A., Castillo, E., Waeber, G., Bergonzelli, G.E., Aubert, J.F., Sutter, E., Nicod, P., Waeber, B., Meda, P. Circulation (1997) [Pubmed]
  22. Influence of the status of the renin-angiotensin system on the effect of cilazapril on neointima formation after vascular injury in rats. Clozel, J.P., Müller, R.K., Roux, S., Fischli, W., Baumgartner, H.R. Circulation (1993) [Pubmed]
  23. Interrelations of the renal kallikrein-kinin system and renal prostaglandins in the conscious rat. Influence of mineralocorticoids. Nasjletti, A., McGiff, J.C., Colina-Chourio, J. Circ. Res. (1978) [Pubmed]
  24. Reversal of cardiac fibrosis in deoxycorticosterone acetate-salt hypertensive rats by inhibition of the renin-angiotensin system. Brown, L., Duce, B., Miric, G., Sernia, C. J. Am. Soc. Nephrol. (1999) [Pubmed]
  25. Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway. Ogata, T., Miyauchi, T., Sakai, S., Takanashi, M., Irukayama-Tomobe, Y., Yamaguchi, I. J. Am. Coll. Cardiol. (2004) [Pubmed]
  26. Increased renal medullary endothelin-1 synthesis in prehypertensive DOCA- and salt-treated rats. Hsieh, T.J., Lin, S.R., Lee, Y.J., Shin, S.J., Lai, Y.H., Hsu, C.H., Tsai, J.H. Am. J. Physiol. Renal Physiol. (2000) [Pubmed]
  27. Renal endothelin receptor type B upregulation in rats with low or high renin hypertension. Brakch, N., Abdel-Sayed, S., Allemandou, F., Wang, Q., Aubert, J.F., Brunner, H.R., Nussberger, J. J. Hypertens. (2004) [Pubmed]
  28. Regulation by sodium intake of type 1 angiotensin II receptor mRNAs in the kidney of Sabra rats. Nicco, C., Martin, H., Yagil, C., Yagil, Y., Bankir, L., Bouby, N. J. Hypertens. (2000) [Pubmed]
  29. Superoxide anion is elevated in sympathetic neurons in DOCA-salt hypertension via activation of NADPH oxidase. Dai, X., Cao, X., Kreulen, D.L. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  30. Mineralocorticoids and glucocorticoids cooperatively increase salt intake and angiotensin II receptor binding in rat brain. Shelat, S.G., King, J.L., Flanagan-Cato, L.M., Fluharty, S.J. Neuroendocrinology (1999) [Pubmed]
  31. Response of a pregnancy-dependent mouse mammary tumor to hormones. Matsuzawa, A., Yamamoto, T. J. Natl. Cancer Inst. (1975) [Pubmed]
  32. Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats. Berecek, K.H., Murray, R.D., Gross, F. Circ. Res. (1980) [Pubmed]
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