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Chemical Compound Review

D-Valsartan     (2R)-3-methyl-2-[pentanoyl- [[4-[2-(2H...

Synonyms: Valsartan, D-, SureCN2328, CHEMBL115622, ANW-49605, CGP-49309, ...
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Disease relevance of valsartan


Psychiatry related information on valsartan


High impact information on valsartan

  • In vitro treatment of younger WKY rat and SHR coronary arteries with the nonpeptide angiotensin II (AT1) receptor antagonist valsartan 10(-5) mol/L (n = 3 for each) fully suppressed contractions to angiotensin II 10(-7) mol/L [9].
  • High glucose-induced JAK2 activation was blunted by both ACE inhibition (100 nmol/l ramipril) and AT1 antagonism (1 mumol/l valsartan), thus revealing that the effects are mediated by autocrine Ang II production [10].
  • Valsartan prevented monocyte/macrophage infiltration, nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) activation, and c-fos expression in dTGR hearts [3].
  • NF-kappaB subunit p65 and TF expression was increased in the endothelium and media of cardiac vessels and markedly reduced by valsartan treatment [3].
  • In the first study arm, Sprague-Dawley rats received a continuous infusion of AGE-modified rat serum albumin (RSA) or unmodified RSA for 4 wk with or without the angiotensin receptor type 1 antagonist valsartan [5].

Chemical compound and disease context of valsartan


Biological context of valsartan

  • Valsartan inhibited the upregulation of NHE-1 mRNA and protein but had no effect on NBC-1 mRNA expression and translation [16].
  • Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure: Valsartan heart failure trial (Val-HeFT) echocardiographic data [17].
  • Consistent with the data on clinical events, patients randomized to valsartan showed improvements in physiologic variables, such as ejection fraction, left ventricular internal diameter in diastole, and plasma neurohormone levels [18].
  • CONCLUSION: These data are consistent with the pharmacokinetics of valsartan in that biliary excretion is the main route of elimination [19].
  • L-NAME 3.7 nmol x kg(-1) x min(-1) improved PBF autoregulation by lowering PBF to the range of 100 to 140 mm Hg of perfusion pressure, and this effect was attenuated or abolished by valsartan in innervated and denervated kidneys, respectively [20].

Anatomical context of valsartan

  • Treatment with valsartan or combination therapy normalized the total and type I collagen (p < 0.001) as well as TGF-beta 1 mRNA level (p < 0.01) in the septum and was associated with the suppression of macrophages and myofibroblasts in the infarct zone (p < 0.01) [21].
  • Angiotensin II receptor blocker valsartan suppresses reactive oxygen species generation in leukocytes, nuclear factor-kappa B, in mononuclear cells of normal subjects: evidence of an antiinflammatory action [22].
  • RESULTS: Valsartan abolished angiotensin II-induced vasoconstriction and, more importantly, also ET-1-induced vasoconstriction in the skin microcirculation (ET-1 placebo versus valsartan, - 33 +/- 10 PU versus +33 +/- 21 PU for CC [P = .02] and -71 +/- 25 PU versus +108 +/- 21 PU for CT/TT [P < .001]) [23].
  • The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days [24].
  • Incubation of myocytes (6-9 h) with the angiotensin II (ATII) receptor blockers saralasin or valsartan (1 microM) significantly augmented these currents [25].

Associations of valsartan with other chemical compounds


Gene context of valsartan


Analytical, diagnostic and therapeutic context of valsartan

  • However, valsartan had no effect on increased filtration fraction associated with an AGE-RSA infusion [5].
  • Exposure to valsartan in patients with mild (n = 6) or moderate (n = 6) impaired liver function (Child's-Pugh classification) and matching (sex, age, and weight) healthy volunteers (n = 12) was studied after oral administration of a single dose of 160 mg valsartan [19].
  • Clinical trials have demonstrated that the combination of valsartan 80 or 160mg with hydrochlorothiazide 12.5 or 25mg is significantly more effective than either drug alone [33].
  • Conversely, a single, exploratory randomised trial demonstrated that the selective AT1R antagonist valsartan significantly reduced stent restenosis after PCI [34].
  • RESULTS: A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats [24].


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  8. Valsartan reduces interleukin-1beta secretion by peripheral blood mononuclear cells in patients with essential hypertension. Li, Q.Z., Deng, Q., Li, J.Q., Yi, G.H., Zhao, S.P. Clin. Chim. Acta (2005) [Pubmed]
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  11. Diuretic and enhanced sodium restriction results in improved antiproteinuric response to RAS blocking agents. Esnault, V.L., Ekhlas, A., Delcroix, C., Moutel, M.G., Nguyen, J.M. J. Am. Soc. Nephrol. (2005) [Pubmed]
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  13. Role of angiotensin receptor subtypes in mesenteric vascular proliferation and hypertrophy. Cao, Z., Dean, R., Wu, L., Casley, D., Cooper, M.E. Hypertension (1999) [Pubmed]
  14. Monocyte infiltration and adhesion molecules in a rat model of high human renin hypertension. Mervaala, E.M., Müller, D.N., Park, J.K., Schmidt, F., Löhn, M., Breu, V., Dragun, D., Ganten, D., Haller, H., Luft, F.C. Hypertension (1999) [Pubmed]
  15. Valsartan/Hydrochlorothiazide: a review of its use in the management of hypertension. Wagstaff, A.J. Drugs (2006) [Pubmed]
  16. Differential effects of angiotensin AT1 and AT2 receptors on the expression, translation and function of the Na+-H+ exchanger and Na+-HCO3- symporter in the rat heart after myocardial infarction. Sandmann, S., Yu, M., Kaschina, E., Blume, A., Bouzinova, E., Aalkjaer, C., Unger, T. J. Am. Coll. Cardiol. (2001) [Pubmed]
  17. Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure: Valsartan heart failure trial (Val-HeFT) echocardiographic data. Wong, M., Staszewsky, L., Latini, R., Barlera, S., Glazer, R., Aknay, N., Hester, A., Anand, I., Cohn, J.N. J. Am. Coll. Cardiol. (2004) [Pubmed]
  18. Effects of valsartan on morbidity and mortality in patients with heart failure not receiving angiotensin-converting enzyme inhibitors. Maggioni, A.P., Anand, I., Gottlieb, S.O., Latini, R., Tognoni, G., Cohn, J.N. J. Am. Coll. Cardiol. (2002) [Pubmed]
  19. Pharmacokinetics of valsartan in patients with liver disease. Brookman, L.J., Rolan, P.E., Benjamin, I.S., Palmer, K.R., Wyld, P.J., Lloyd, P., Flesch, G., Waldmeier, F., Sioufi, A., Mullins, F. Clin. Pharmacol. Ther. (1997) [Pubmed]
  20. Interactions between nitric oxide and angiotensin II on renal cortical and papillary blood flow. Madrid, M.I., García-Salom, M., Tornel, J., de Gasparo, M., Fenoy, F.J. Hypertension (1997) [Pubmed]
  21. Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction. Yu, C.M., Tipoe, G.L., Wing-Hon Lai, K., Lau, C.P. J. Am. Coll. Cardiol. (2001) [Pubmed]
  22. Angiotensin II receptor blocker valsartan suppresses reactive oxygen species generation in leukocytes, nuclear factor-kappa B, in mononuclear cells of normal subjects: evidence of an antiinflammatory action. Dandona, P., Kumar, V., Aljada, A., Ghanim, H., Syed, T., Hofmayer, D., Mohanty, P., Tripathy, D., Garg, R. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
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  24. Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats. Chan, P., Wong, K.L., Liu, I.M., Tzeng, T.F., Yang, T.L., Cheng, J.T. J. Hypertens. (2003) [Pubmed]
  25. Inhibition of the formation or action of angiotensin II reverses attenuated K+ currents in type 1 and type 2 diabetes. Shimoni, Y. J. Physiol. (Lond.) (2001) [Pubmed]
  26. Pharmacologic demonstration of the synergistic effects of a combination of the renin inhibitor aliskiren and the AT1 receptor antagonist valsartan on the angiotensin II-renin feedback interruption. Azizi, M., Ménard, J., Bissery, A., Guyenne, T.T., Bura-Rivière, A., Vaidyanathan, S., Camisasca, R.P. J. Am. Soc. Nephrol. (2004) [Pubmed]
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  28. Regulation of collagen synthesis in mouse skin fibroblasts by distinct angiotensin II receptor subtypes. Min, L.J., Cui, T.X., Yahata, Y., Yamasaki, K., Shiuchi, T., Liu, H.W., Chen, R., Li, J.M., Okumura, M., Jinno, T., Wu, L., Iwai, M., Nahmias, C., Hashimoto, K., Horiuchi, M. Endocrinology (2004) [Pubmed]
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  30. Identification of cytochrome P450 forms involved in the 4-hydroxylation of valsartan, a potent and specific angiotensin II receptor antagonist, in human liver microsomes. Nakashima, A., Kawashita, H., Masuda, N., Saxer, C., Niina, M., Nagae, Y., Iwasaki, K. Xenobiotica (2005) [Pubmed]
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  32. Angiotensin II regulates phosphoinositide 3 kinase/Akt cascade via a negative crosstalk between AT1 and AT2 receptors in skin fibroblasts of human hypertrophic scars. Liu, H.W., Cheng, B., Yu, W.L., Sun, R.X., Zeng, D., Wang, J., Liao, Y.X., Fu, X.B. Life Sci. (2006) [Pubmed]
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