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Effects of some angiotensin‐converting enzyme inhibitors and angiotensin II receptor blockers on experimental inflammations
Author(s) -
Magyar Ioan,
Cret Mihai,
Cuparencu Barbu
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb567
Subject(s) - enalapril , quinapril , lisinopril , valsartan , angiotensin converting enzyme , proinflammatory cytokine , captopril , angiotensin ii , angiotensin ii receptor type 1 , bradykinin , pharmacology , chemistry , medicine , ace inhibitor , endocrinology , receptor , inflammation , blood pressure
Method The experiments were carried out in Wistar albino rats, weighing 150–200 g. The inflammations were induced as folows: 1. the hind paw edema evoked by the intraplantar injection of 0.1 mL from a 10% aqueos kaolin suspension; the measurements of the paw volume increases were performed plethismometrically; 2. the insertion of a cotton pellet, weighing 50 mg into the scapulo‐humeral region. The following bood inflammatory markers were measured: fibrinogen and C‐reactive protein (CRP). The tested drugs by intraperitoneally route were: captopril (0.4–4.0–6.0 mg), enalapril (0.2–2.0–4.0 mg), lisinopril (0.2–2.0–4.0 mg), quinapril (0.2–2.0–4.0 mg) and valsartan (4.0–8.0–16.0 mg). The statistical evaluation was carried out by chi square and “size effect” procedures. Results All ACEI exhibited in a dose‐dependent and a time‐related manner a proinflammatory activity. The most active compounds were: quinapril and enalapril and lisinopril. Valsartan was ineffective. Fibrinogen and CRP blood levels were increased by all ACEI. However, no clear dose‐response relationships might be seen. Discussion Conclusion From these data it may be inferred that the proinflammatory activity of ACEI was due to an accumulation of bradykinin, a phlogogenic peptide. It is well known that the converting enzyme, besides its splitting effect of angiotensin I, leading to the genesis of angiotensin II has a kininase activity.