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Chemical Compound Review

Quinazil     (3S)-2-[(2S)-2-[[(1S)-1- ethoxycarbonyl-3...

Synonyms: Accupro, quinapril, Quinaprilum, QUINAPRIL HCL, CHEMBL1592, ...
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Disease relevance of C07398


Psychiatry related information on C07398


High impact information on C07398


Chemical compound and disease context of C07398


Biological context of C07398


Anatomical context of C07398


Associations of C07398 with other chemical compounds


Gene context of C07398

  • After treatment with quinapril, the basal and LPS-induced expressions of iNOS in SHR were significantly attenuated [21].
  • Four weeks of therapy with quinapril attenuated the positive inotropic effects of ET-1 and prevented the increase in ET-A receptor mRNA [22].
  • RESULTS: Simvastatin treatment significantly decreased serum CRP and TNF-a [from 14 +/- 6 to 7 +/- 3 mg/l (p = 0.025) and 30 +/- 5 to 16 +/- 4 pg/ml (p = 0.012), respectively], while quinapril had no significant changes in these 2 measures [23].
  • DiC8 also prevented the augmentation of Kv4.2 density by quinapril [24].
  • Although quinapril did not restore the effects of ET-B receptor stimulation or prevent the increase in ET-B mRNA, it did restore cardiac ecNOS protein expression [22].

Analytical, diagnostic and therapeutic context of C07398

  • The rapidity of drug dose escalation influences blood pressure response and adverse effects burden in patients with hypertension: the Quinapril Titration Interval Management Evaluation (ATIME) Study. ATIME Research Group [25].
  • CONCLUSIONS: Our findings suggest that quinapril significantly increases parasympathetic activity in patients with DAN 3 months after treatment initiation and sustains this effect until the 6th month [26].
  • To assess whether timing of administration can influence the antihypertensive effect of quinapril, 18 patients with hypertension were studied with noninvasive ambulatory blood pressure monitoring [27].
  • Relationships between glomerular dynamics and renal injury, micropuncture and histological studies were assessed in 73 week-old normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats divided into untreated and angiotension-converting enzyme inhibitor-treated (quinapril; 3 mg/kg/day; for 3 weeks) groups [28].
  • Therefore, the goal of this double-blind, randomized study was to compare the antihypertensive and renal effects of the ACE inhibitor quinapril with those of the beta-blocker atenolol in renal allograft recipients in whom hypertension developed 6 to 12 weeks after transplantation [10].


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  14. Modulation of incipient glomerular lesions in experimental diabetic nephropathy by hypotensive and subhypotensive dosages of an ACE inhibitor. Fabris, B., Candido, R., Carraro, M., Fior, F., Artero, M., Zennaro, C., Cattin, M.R., Fiorotto, A., Bortoletto, M., Millevoi, C., Bardelli, M., Faccini, L., Carretta, R. Diabetes (2001) [Pubmed]
  15. ACE inhibitor quinapril reduces the arterial expression of NF-kappaB-dependent proinflammatory factors but not of collagen I in a rabbit model of atherosclerosis. Hernández-Presa, M.A., Bustos, C., Ortego, M., Tuñón, J., Ortega, L., Egido, J. Am. J. Pathol. (1998) [Pubmed]
  16. Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis. Ruiz-Ortega, M., Bustos, C., Hernández-Presa, M.A., Lorenzo, O., Plaza, J.J., Egido, J. J. Immunol. (1998) [Pubmed]
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  18. Potentiation of bradykinin-induced tissue plasminogen activator release by angiotensin-converting enzyme inhibition. Labinjoh, C., Newby, D.E., Pellegrini, M.P., Johnston, N.R., Boon, N.A., Webb, D.J. J. Am. Coll. Cardiol. (2001) [Pubmed]
  19. Angiotensin converting enzyme inhibition prevents the increase in aortic collagen in rats. Albaladejo, P., Bouaziz, H., Duriez, M., Gohlke, P., Levy, B.I., Safar, M.E., Benetos, A. Hypertension (1994) [Pubmed]
  20. 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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