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The preventive effect of captopril or enalapril on reperfusion injury of the kidney of rats is independent of angiotensin II AT1 receptors
Author(s) -
PazokiToroudi Hamid Reza,
Hesami Ali,
Vahidi Simin,
Sahebjam Farhad,
Seifi Behjat,
Djahanguiri Bijan
Publication year - 2003
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1046/j.1472-8206.2003.00188.x
Subject(s) - enalapril , losartan , captopril , angiotensin ii receptor type 1 , angiotensin converting enzyme , renin–angiotensin system , angiotensin ii , medicine , kidney , ace inhibitor , angiotensin receptor , pharmacology , endocrinology , receptor , blood pressure
Occlusion of the artery of organs results in ischaemia. The opening of occluded artery results in tissue lesion identified as reperfusion injury (RI). Renin–angiotensin system seems to be involved in the RI. In this study we assessed the effects of different doses of two inhibitors of angiotensin converting enzyme (captopril or enalapril) and an angiotensin receptor type 1 (AT1) receptor blocker (losartan) in the RI of the kidney of rats. Female rats of 200–250 g were anaesthetized and used for RI studies. Different doses of captopril (5, 20 and 80 mg/kg), enalapril (1, 4 and 16 mg/kg) and/or losartan (5, 10 and 20 mg/kg) were used (s.c.) 120 min prior to the initiation of RI. Kidneys were removed and checked histologically for the presence and the grading of ischaemic injury. Appropriate controls were used as well. RI produced lesions comparable with that of ischaemia. Different doses of captopril or enalapril prevented these lesions. This is suggestive of the involvement of renin–angiotensin system in the RI. Different doses of losartan failed to prevent RI lesions which suggest that the effect of captopril or enalapril are not mediated through the AT1 receptors. Further studies on the involvement of AT2 receptor or other independent mechanisms are suggested.