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RENAL ISCHEMIA/REPERFUSION INDUCED CARDIAC HYPERTROPHY IN MICE: CONTRIBUTION OF CARDIAC RENIN ANGIOTENSIN SYSTEM
Author(s) -
Abrahao Mariana Vieira,
Carneiro-Ramos Marcela Sorelli
Publication year - 2012
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.26.1_supplement.lb640
Subject(s) - medicine , losartan , ischemia , kidney , endocrinology , renin–angiotensin system , muscle hypertrophy , renal ischemia , angiotensin ii , angiotensin ii receptor type 1 , cardiac hypertrophy , cardiology , reperfusion injury , blood pressure
Objectives This study aims to characterize the role of cardiac RAS in models of cardiac hypertrophy induced by ischemic renal injury in mice. Methods C57bl/6J mice were subjected to unilateral 60 min kidney ischemia, followed by reperfusion of 12, 15 and 20 days. The animals were randomized and equally divided into three groups: (i) untreated, (ii) treated with Losartan (Los ‐ 10mg/kg/day) for 5 days before ischemia protocol and (iii) treated with Los for 5 days after, with respective sham controls for all groups. Levels of urea were measured to confirm renal failure and gene expression were analyzed by real time PCR. Results The heart weight/body weight or tibia length ratios and mRNA ANF were increased on 12 and 15 days mice untreated with Los. Pre and post treatment with Los were able to prevent and reverse, respectively, the increase on mRNA ANF levels induced by renal/ischemia protocol only at the 15 days time point (p<0.01). Cardiac mRNA AT1a levels were decreased after post treatment with Los after 15 days of renal ischemia when compared to 15 days untreated mice. Conclusion The renal ischemia/reperfusion model was able to induce cardiac hypertrophy that was prevented and reversed with Los administration. Moreover, cardiac mRNA AT1 levels are decreased in 15 days mice post treated with Los, suggesting a local modulation of cardiac RAS in this cardiac hypertrophy model. Financial Support: FAPESP, CNPq and UFABC.