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Chemical Compound Review

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

Synonyms: enalapril, SureCN18, CHEMBL578, Enalapril (TN), AC1NTUS5, ...
 
 
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Disease relevance of enalapril

  • To determine the physiological relevance of the renin-angiotensin system in the pituitary hormone response to stress in humans, we created significant inhibition of ACE by administering a clinically used dose (10 mg) of enalapril (E) 4 h before measuring the stress hormone responses to insulin-induced hypoglycemia [1].
  • Compared to CON, significant hypertension was prevented, kidney weight was lower and there was less proteinuria in HHR, CAP and ENP rats followed for 30 weeks after UNX [2].
  • ENA treatment achieved control of both systemic and glomerular hypertension, maintenance of glomerular hyperfiltration and hyperperfusion, increased ultrafiltration coefficient(Kf), and long-term protection against UpV and FGS [3].
  • The RAS blockade by ENA or ENA + CSN in rats receiving AA did not result in any statistical difference in terms of renal failure, proteinuria, and interstitial fibrosis on day 35 or 65 [4].
  • However, treatment with subantihypertensive doses of ENA and RAM had no effect on MAP, LV/body weight ratio, PPdil, or PPmax [5].
 

High impact information on enalapril

  • Micropuncture studies of rats performed using a similar treatment protocol demonstrated greater reduction of glomerular capillary hydraulic pressure with OMA than with ENA, at similar mean arterial pressures [6].
  • It is concluded that, in this model, OMA affords greater long-term renoprotection than ENA when doses are adjusted to yield equivalent control of SBP [6].
  • These differences in PRL responses appeared to be due primarily to substantial decreases in PRL responses with E in three of the eight subjects [1].
  • On day 35, the monocytes/macrophages infiltration was significantly decreased by two-fold when ENA (P < 0.01) or ENA + CSN (P < 0.01) was given from day 0 [4].
  • Renal cortex mRNA levels (determined by competitive RT-PCR) for transforming growth factor (TGF)-beta1 and monocyte chemoattractant protein (MCP)-1 were elevated in Csn and Ena at 12 wk and remained higher at 24 wk vs. sham [7].
 

Chemical compound and disease context of enalapril

 

Biological context of enalapril

  • Despite control of systolic blood pressure (SBP; 24 wk: Csn = 143 +/- 9; Ena = 148 +/- 8 mmHg), urinary protein excretion rates (U(pr)V) increased over 24 wk (Csn = 92 +/- 10; Ena = 99 +/- 8mg/day) [7].
  • An increased heart rate was seen after administration of either T4 alone or T4 in combination with either Los or Ena [11].
  • EP administration had no effect on water intake, ambient efPosm and PAVP, and the AVP response to osmotic loading in rats fed the control diet [12].
  • Regression of cardiovascular changes occurred as reduction in left ventricular (LV) weight/body weight ratio (25 and 21% for ENA and RAM, respectively), reduction in perfusion pressure at maximal vasodilation of the perfused hindquarter (PPdil, 17 and 17%), and reduction in maximal developed pressure (PPmax, 13 and 17%) [5].
  • In patients with proteinuria and poorly controlled diabetes, in response to E-induced efferent arteriolar dilation, there is a decrease in GFR and an increase in PI which indicates a fall in filtration and renal blood flow [13].
 

Anatomical context of enalapril

  • ACE activity of the cerebrum was significantly decreased in the Enal group [14].
 

Associations of enalapril with other chemical compounds

 

Gene context of enalapril

  • Ena and Prop inhibited the increase in HW or HW/BW in hyperthyroid rats [11].
  • Our study indicates that protein metabolism in nephrotic patients is better maintained with HPD + ENAL than with LPD alone [16].
  • These findings were accompanied by an increase in the percent of juxtaglomerular apparatuses (JGAs) containing renin mRNA (71 +/- 2.2 vs. 49 +/- 2.9%; E vs. C, P less than 0.0001) [17].
 

Analytical, diagnostic and therapeutic context of enalapril

  • Micropuncture studies performed five weeks after UNX in four additional groups of CON, HHR, CAP and ENP rats revealed that glomerular capillary pressure was elevated in CON and reduced by all three drug regimens [2].
  • Sustained AF requiring cardioversion for termination was induced in 0% of unpaced dogs vs. 33% of CariL, 33% of CariH, 33% of E, and 43% of control dogs [18].
  • Two days later, renal scintigraphy was repeated after oral administration of E [13].

References

  1. Effect of angiotensin-converting enzyme inhibition on pituitary hormone responses to insulin-induced hypoglycemia in humans. Winer, L.M., Molteni, A., Molitch, M.E. J. Clin. Endocrinol. Metab. (1990) [Pubmed]
  2. Renal vascular effects of antihypertensive therapy in uninephrectomized SHR. Dworkin, L.D., Grosser, M., Feiner, H.D., Ullian, M., Parker, M. Kidney Int. (1989) [Pubmed]
  3. Modulation of glomerular hypertension defines susceptibility to progressive glomerular injury. Simons, J.L., Provoost, A.P., Anderson, S., Rennke, H.G., Troy, J.L., Brenner, B.M. Kidney Int. (1994) [Pubmed]
  4. The renin-angiotensin system blockade does not prevent renal interstitial fibrosis induced by aristolochic acids. Debelle, F.D., Nortier, J.L., Husson, C.P., De Prez, E.G., Vienne, A.R., Rombaut, K., Salmon, I.J., Deschodt-Lanckman, M.M., Vanherweghem, J.L. Kidney Int. (2004) [Pubmed]
  5. Therapeutic, but not low-dose, angiotensin-converting enzyme inhibition causes regression of cardiovascular changes in spontaneously hypertensive rats. Wahlander, H., Sohtell, M., Wickman, A., Nilsson, A., Friberg, P. J. Cardiovasc. Pharmacol. (1996) [Pubmed]
  6. Vasopeptidase inhibition affords greater renoprotection than angiotensin-converting enzyme inhibition alone. Taal, M.W., Nenov, V.D., Wong, W., Satyal, S.R., Sakharova, O., Choi, J.H., Troy, J.L., Brenner, B.M. J. Am. Soc. Nephrol. (2001) [Pubmed]
  7. Mechanisms underlying renoprotection during renin-angiotensin system blockade. Taal, M.W., Chertow, G.M., Rennke, H.G., Gurnani, A., Jiang, T., Shahsafaei, A., Troy, J.L., Brenner, B.M., Mackenzie, H.S. Am. J. Physiol. Renal Physiol. (2001) [Pubmed]
  8. Effect of angiotensin convertase inhibitors and AT1 angiotensin receptor antagonists on the development of oxidative stress in the kidney of diabetic rats. Kedziora-Kornatowska, K. Clin. Chim. Acta (1999) [Pubmed]
  9. Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats. Wojewódzka-Zelezniakowicz, M., Chabielska, E., Mogielnicki, A., Kramkowski, K., Karp, A., Opadczuk, A., Domaniewski, T., Malinowska-Zaprzałka, M., Buczko, W. J. Physiol. Pharmacol. (2006) [Pubmed]
  10. Lipid peroxidation and activities of antioxidant enzymes in the diabetic kidney: effect of treatment with angiotensin convertase inhibitors. Kedziora-Kornatowska, K.Z., Luciak, M., Paszkowski, J. IUBMB Life (2000) [Pubmed]
  11. Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling. Hu, L.W., Benvenuti, L.A., Liberti, E.A., Carneiro-Ramos, M.S., Barreto-Chaves, M.L. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2003) [Pubmed]
  12. Reset of the osmotic threshold for vasopressin in rats fed a low NaCl, K-free diet. Peterson, L.N., Mathur, S., Borzecki, J.S. Can. J. Physiol. Pharmacol. (1992) [Pubmed]
  13. Scintigraphic evaluation of functional renal reserve using angiotensin-converting enzyme inhibition in patients with type II diabetes mellitus. Erbas, B., Erbas, T., Akalin, S., Varoglu, E., Koray, Z., Bekdik, C.F. American journal of nephrology. (1993) [Pubmed]
  14. The influence of chronic antihypertensive treatment on the central pressor response in SHR. Lin, Y., Tsuchihashi, T., Kagiyama, S., Matsumura, K., Abe, I. Hypertens. Res. (2001) [Pubmed]
  15. Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors. Liao, S., Miralles, M., Kelley, B.J., Curci, J.A., Borhani, M., Thompson, R.W. J. Vasc. Surg. (2001) [Pubmed]
  16. Effectiveness of dietary protein augmentation associated with angiotensin-converting enzyme inhibition in the management of the nephrotic syndrome. Garini, G., Mazzi, A., Allegri, L., Buzio, C., Borghetti, A. Mineral and electrolyte metabolism. (1996) [Pubmed]
  17. Recruitment of renin gene-expressing cells in adult rat kidneys. Gomez, R.A., Chevalier, R.L., Everett, A.D., Elwood, J.P., Peach, M.J., Lynch, K.R., Carey, R.M. Am. J. Physiol. (1990) [Pubmed]
  18. Effects of inhibiting Na(+)/H(+)-exchange or angiotensin converting enzyme on atrial tachycardia-induced remodeling. Shinagawa, K., Mitamura, H., Ogawa, S., Nattel, S. Cardiovasc. Res. (2002) [Pubmed]
 
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