Abstract
MethodThe 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.ResultsAll 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.DiscussionConclusionFrom 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.
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