The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

Remikiren     (2S)-2-benzyl-N-[(1S)-1- [[(2R,3S,4R)-1...

Synonyms: AC1NUWCS, CHEMBL31601, SureCN156394, CCRIS 6519, CHEBI:142751, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Remikiren

  • Forty-nine patients with moderate essential hypertension were randomly assigned to three groups that entered an 8-day double-blind oral treatment period: daily administration of placebo (group A), 300 mg Ro 42-5892 (group B), or 600 mg Ro 42-5892 (group C) [1].
  • Thus, side effects such as rash, angioneurotic edema or cough, which have been attributed to bradykinin accumulation by ACE inhibitors, may not occur with the use of specific renin inhibitors such as Ro 42-5892 [2].
  • METHODS: The effect of 8 days of treatment with remikiren 600 mg o.i.d. on blood pressure, renal haemodynamics, and proteinuria was studied in 14 hypertensive patients with normal or impaired renal function.The study was conducted on an ambulatory in-hospital basis and was designed in a single-blind, longitudinal order [3].
  • This effect was observed not only in strains TA1538 and TA98 but also in the standard Salmonella tester strains where the spontaneous mutant frequency was not increased by Ro 42-5892 [4].

High impact information on Remikiren

  • METHODS AND RESULTS: Twenty-four normotensive male volunteers homozygous for the ACE I/D polymorphism (12 DD and 12 II) received a renin inhibitor infusion (remikiren 0.1 for 130 minutes) to suppress endogenous Ang I and Ang II production [5].
  • Captopril, but not Ro 42-5892, increased forearm blood flow (2.4 +/- 0.8 versus 1.9 +/- 0.8 ml/min/100 ml, p less than 0.01) and significantly enhanced the increase of forearm blood flow to brachial artery infusions of bradykinin (0.15, 1.5, 5, 15, and 50 ng/min/100 ml; 5 minutes each) from 744 +/- 632% to 1,383 +/- 514% (p less than 0.01) [6].
  • The remikiren-induced rise in ERPF correlated (r = .68, P < .01) with the fall in MAP (114 +/- 2 to 110 +/- 2 mm Hg) [7].
  • Four hours after the last oral drug intake, placebo was administered intravenously to subjects in group A and 100 mg Ro 42-5892 was administered intravenously to subjects in groups B and C. Sitting systolic and diastolic blood pressures were measured on days 1 and 8 with a blood pressure device [1].
  • Efficacy and tolerability of the renin inhibitor Ro 42-5892 in patients with hypertension [1].

Chemical compound and disease context of Remikiren

  • RESULTS: Daytime proteinuria declined from 0.29 +/- 0.15 to 0.22 +/- 0.11 g/h (P < 0.05) during remikiren and from 0.33 +/- 0.14 to 0.16 +/- 0.08 g/h (P < 0.05) during trandolapril [8].
  • When Ro 42-5892 was given, 1 mg/kg intravenously in 10 min, to subjects with hypertension, it appeared that plasma ANG I and II returned to baseline after 6-8 h, whereas PRA measured in the presence of PMSF and 8-OHQ was still suppressed [9].

Biological context of Remikiren


Anatomical context of Remikiren

  • The primate microsomes also produced more of the remaining mono- and di-hydroxy products, suggesting that metabolites make little contribution to the oral activity of remikiren which is observed in these species in vivo [14].

Associations of Remikiren with other chemical compounds


Gene context of Remikiren

  • Infused hREN blocked with remikiren resulted in T1/2beta and MCR values that were not different from control values [18].
  • The goal of the present study was to characterize the new renin inhibitor Ro 42-5892 in vitro and in vivo [11].
  • We used human and mouse renin, transgenic human angiotensinogen, and the human renin inhibitor Ro 42-5892 to determine human- and rat-specific plasma angiotensinogen concentrations, renin activity, and renin concentration [19].
  • MATERIALS AND METHODS: Renal hemodynamics, and the effects of single (n = 17) and multiple doses (n = 8, 8 days) of remikiren (600 mg day-1) on sodium excretion were studied under conditions of carefully controlled sodium balance [20].
  • In contrast, on the last day of active treatment, a larger, faster and longer decrease in sitting DBP was observed in the Ro 42-5892 group [21].

Analytical, diagnostic and therapeutic context of Remikiren


  1. Efficacy and tolerability of the renin inhibitor Ro 42-5892 in patients with hypertension. Rongen, G.A., Lenders, J.W., Kleinbloesem, C.H., Weber, C., Welker, H., Fahrner, E., Pozenel, H., Woittiez, A.J., Haug, G., Buchmann, M.S. Clin. Pharmacol. Ther. (1993) [Pubmed]
  2. A comparison of the effects of renin inhibition and angiotensin converting enzyme inhibition upon bradykinin potentiation. Véniant, M., Clozel, J.P., Fischli, W. J. Hypertens. (1992) [Pubmed]
  3. Renal and systemic effects of continued treatment with renin inhibitor remikiren in hypertensive patients with normal and impaired renal function. van Paassen, P., de Zeeuw, D., Navis, G., de Jong, P.E. Nephrol. Dial. Transplant. (2000) [Pubmed]
  4. Renin inhibitors as an example of presumptive irrelevant positive findings in the Salmonella/mammalian microsome assay (Ames test). Albertini, S., Gocke, E. Mutat. Res. (1993) [Pubmed]
  5. Angiotensin-converting enzyme gene polymorphism has no influence on the circulating renin-angiotensin-aldosterone system or blood pressure in normotensive subjects. Lachurié, M.L., Azizi, M., Guyene, T.T., Alhenc-Gelas, F., Ménard, J. Circulation (1995) [Pubmed]
  6. Blood pressure control by the renin-angiotensin system in normotensive subjects. Assessment by angiotensin converting enzyme and renin inhibition. Kiowski, W., Linder, L., Kleinbloesem, C., van Brummelen, P., Bühler, F.R. Circulation (1992) [Pubmed]
  7. Does the renin-angiotensin system determine the renal and systemic hemodynamic response to sodium in patients with essential hypertension? van Paassen, P., de Zeeuw, D., Navis, G., de Jong, P.E. Hypertension (1996) [Pubmed]
  8. Is the antiproteinuric response to inhibition of the renin-angiotensin system less effective during the night? Buter, H., Hemmelder, M.H., van Paassen, P., Navis, G., de Zeeuw, D., de Jong, P.E. Nephrol. Dial. Transplant. (1997) [Pubmed]
  9. Nonparallel effects of renin inhibitor treatment on plasma renin activity and angiotensins I and II in hypertensive subjects. An assay-related artifact. Derkx, F.H., van den Meiracker, A.H., Fischli, W., Admiraal, P.J., Man in't Veld, A.J., van Brummelen, P., Schalekamp, M.A. Am. J. Hypertens. (1991) [Pubmed]
  10. Hemodynamics, biochemical effects, and pharmacokinetics of the renin inhibitor remikiren in healthy human subjects. Kleinbloesem, C.H., Weber, C., Fahrner, E., Dellenbach, M., Welker, H., Schröter, V., Belz, G.G. Clin. Pharmacol. Ther. (1993) [Pubmed]
  11. Ro 42-5892 is a potent orally active renin inhibitor in primates. Fischli, W., Clozel, J.P., el Amrani, K., Wostl, W., Neidhart, W., Stadler, H., Branca, Q. Hypertension (1991) [Pubmed]
  12. Specific receptor binding of renin on human mesangial cells in culture increases plasminogen activator inhibitor-1 antigen. Nguyen, G., Delarue, F., Berrou, J., Rondeau, E., Sraer, J.D. Kidney Int. (1996) [Pubmed]
  13. Assessment of the role of the renin-angiotensin system in cardiac contractility utilizing the renin inhibitor remikiren. van Kats, J.P., Sassen, L.M., Danser, A.H., Polak, M.P., Soei, L.K., Derkx, F.H., Schalekamp, M.A., Verdouw, P.D. Br. J. Pharmacol. (1996) [Pubmed]
  14. Excretion and metabolism of remikiren, a potent orally active inhibitor of primate renin. Jauch, R., Schmid, P., Fischli, W., Meister, W., Maurer, R., Wendt, G. Xenobiotica (1996) [Pubmed]
  15. Effects of renin-angiotensin system blockade in guinea pigs. Véniant, M., Clozel, J.P., Hess, P., Fischli, W. Hypertension (1992) [Pubmed]
  16. Comparison of blood pressure and angiotensin responses to the renin inhibitor Ro 42-5892 and the angiotensin converting enzyme inhibitor enalapril in essential hypertension. van den Meiracker, A.H., Admiraal, P.J., Derkx, F.H., Kleinbloesem, C., Man in 't Veld, A.J., van Brummelen, P., Mulder, P., Schalekamp, M.A. J. Hypertens. (1993) [Pubmed]
  17. Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, angiotensin II-independent mechanisms. Huang, Y., Wongamorntham, S., Kasting, J., McQuillan, D., Owens, R.T., Yu, L., Noble, N.A., Border, W. Kidney Int. (2006) [Pubmed]
  18. Angiotensinogen concentrations and renin clearance : implications for blood pressure regulation. Bohlender, J., Ménard, J., Ganten, D., Luft, F.C. Hypertension (2000) [Pubmed]
  19. Human renin-dependent hypertension in rats transgenic for human angiotensinogen. Bohlender, J., Ménard, J., Wagner, J., Luft, F.C., Ganten, D. Hypertension (1996) [Pubmed]
  20. Pretreatment renal vascular tone predicts the effect of specific renin inhibition on natriuresis in essential hypertension. van Paassen, P., Navis, G.J., De Jong, P.E., De Zeeuw, D. Eur. J. Clin. Invest. (1999) [Pubmed]
  21. Time dependency of the antihypertensive efficacy of the new renin inhibitor Ro 42-5892. Viskoper, R.J., Charlon, V., Laszt, A., Yosefy, C., Bock, J., Landau, M., Kobrin, I. Journal of human hypertension. (1994) [Pubmed]
  22. Neurohormonal and blood pressure responses to low-dose infusion of an orally active renin inhibitor, Ro 42-5892, in salt-replete men. Doig, J.K., MacFadyen, R.J., Meredith, P.A., Fischli, W., Reid, J.L. J. Cardiovasc. Pharmacol. (1992) [Pubmed]
  23. Distribution of remikiren, a potent orally active inhibitor of human renin, in laboratory animals. Richter, W.F., Whitby, B.R., Chou, R.C. Xenobiotica (1996) [Pubmed]
WikiGenes - Universities