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Chemical Compound Review

SureCN668526     9-[(4-dimethylamino-3- methyl...

Synonyms: AG-K-52705, ACMC-20d0z4, KST-1B0181, AC1L1IRD, CTK0H8247, ...
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Disease relevance of PD 123319


High impact information on PD 123319

  • L-arginine (L-ARG) given intravenously or interstitially enhanced net fluid absorption and cGMP formation, which were completely blocked by the nitric oxide (NO) synthase inhibitor, N-nitro-L-arginine methylester (L-NAME), but not by the specific AT2 receptor antagonist, PD-123319 (PD) [6].
  • In nonfailing hearts, 69 +/- 4% of binding sites were blocked by the subtype-2-specific inhibitor PD 123319 and were therefore classified as AT2; 33 +/- 5% were blocked by the subtype-1-specific inhibitor DUP 753 and thus classified as subtype 1 [7].
  • Moreover, treatment with the selective AT1 antagonist CV-11974 before injury significantly decreased the formation of neointima in only WT mice, whereas treatment with the selective AT2 antagonist PD-123319 before injury had no effects in both animal groups [8].
  • Valsartan, a specific AT1 receptor antagonist inhibited Ang II binding, whereas PD 123319, an AT2 receptor antagonist did not [9].
  • This stimulatory effect of Ang II on Erk1 and Erk2 activities was potentiated by blockade of AT2 receptors with (S)-1-[4-(dimethylamino)-3-methylphenyl]methyl-5-(diphenylacetyl)- 4, 5,6,7-tetrahydro-1H-imidazo[4,5-C]pyridine-6-carboxylic acid (PD 123319, 1 microM) [10].

Chemical compound and disease context of PD 123319


Biological context of PD 123319


Anatomical context of PD 123319


Associations of PD 123319 with other chemical compounds


Gene context of PD 123319

  • In contrast, the AT2 receptor analogues PD-123319 and CGP-42112 at concentrations < 10(-6) M had no effect on ANG II binding [25].
  • The residual constrictor effect observed during AT1 receptor blockade and sensitive to PD 123319 appears to be mediated by a non-AT1 receptor [14].
  • The selective AT2 receptor ligand, CGP 42112A, antagonized AII-induced [3H]-thymidine incorporation with an IC50 of 6.3 +/- 1.3 microM while the AT2/AT1B receptor antagonist, PD 123319, was found to be almost inactive (IC50 > 10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)[26]
  • Co-incubation with both losartan and PD-123319 resulted in a decrease of ERK and p38 activities in cardiomyocytes [27].
  • The binding of [125I]Sar1-angiotensin II was completely displaced by the AT1 antagonist losartan but not by the AT2 receptor ligand PD 123319, confirming the expression of angiotensin II AT1 receptors in NCI-H295 cells [28].

Analytical, diagnostic and therapeutic context of PD 123319


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  19. Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor. Olson, S., Oeckler, R., Li, X., Du, L., Traganos, F., Zhao, X., Burke-Wolin, T. Am. J. Physiol. Lung Cell Mol. Physiol. (2004) [Pubmed]
  20. ANG II type 2 receptor regulates smooth muscle growth and force generation in late fetal mouse development. Perlegas, D., Xie, H., Sinha, S., Somlyo, A.V., Owens, G.K. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
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  24. Angiotensin II AT2 receptor stimulation extends the upper limit of cerebral blood flow autoregulation: agonist effects of CGP 42112 and PD 123319. Näveri, L., Strömberg, C., Saavedra, J.M. J. Cereb. Blood Flow Metab. (1994) [Pubmed]
  25. Regulation of angiotensin II receptor AT1 subtypes in renal afferent arterioles during chronic changes in sodium diet. Ruan, X., Wagner, C., Chatziantoniou, C., Kurtz, A., Arendshorst, W.J. J. Clin. Invest. (1997) [Pubmed]
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  28. Local renin-angiotensin system is involved in K+-induced aldosterone secretion from human adrenocortical NCI-H295 cells. Hilbers, U., Peters, J., Bornstein, S.R., Correa, F.M., Jöhren, O., Saavedra, J.M., Ehrhart-Bornstein, M. Hypertension (1999) [Pubmed]
  29. The influence of candesartan and PD123319 on responses to angiotensin II in the hindquarters vascular bed of the rat. Champion, H.C., Bivalacqua, T.J., Lambert, D.G., McNamara, D.B., Kadowitz, P.J. J. Am. Soc. Nephrol. (1999) [Pubmed]
  30. Nonpeptide angiotensin AT1 and AT2 receptor ligands modulate the upper limit of cerebral blood flow autoregulation in rats. Strömberg, C., Näveri, L., Saavedra, J.M. J. Cereb. Blood Flow Metab. (1993) [Pubmed]
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