Premium
Role of Renin Angiotensin System inhibitors on Toll‐like receptors expression in cardiac hypertrophy induced by renal ischemia/reperfusion
Author(s) -
Abrahão Mariana,
CarneiroRamos Marcela Sorelli
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.386.6
Subject(s) - losartan , renin–angiotensin system , medicine , enalapril , muscle hypertrophy , receptor , endocrinology , renal ischemia , ischemia , gene expression , kidney , cardiac hypertrophy , angiotensin ii , reperfusion injury , biology , angiotensin converting enzyme , gene , blood pressure , biochemistry
Objective The heart is a target organ of many regulatory systems that modulates heart trophism, such as cardiac renin‐angiotensin system (RAS). Literature data confirm the direct relationship between inflammatory responses, Toll‐Like receptors (TLR) and many cardiovascular diseases. This work aims to investigate the role of RAS inhibitors on TLR expression in a cardiac hypertrophy model induced by renal ischemia/reperfusion. Methods C57bl/6 young, male mice (n=72) were treated with Losartan (Los ‐ 10 mg/kg/day) or Enalapril (Ena ‐ 40 mg/kg/day) for 5 days before or after surgery, and kept under observation for 12, 15 or 20 days to investigate the role of TLR in cardiac hypertrophy, evaluated by morphologic parameters and gene expression. Results Our model was able to induce cardiac hypertrophy in 12d mice that was prevented and reversed with Los and Ena administration based on ANF/α‐actin gene expression. TLR gene expression was evaluated in animal treated with Los and Ena, that were able to reduce TLR mRNA levels in 15d and 20d mice, respectively. Conclusion Taken together our data suggest an important role for local RAS as a modulator of cardiac hypertrophy through regulation of TLR expression. Financial Support: FAPESP and UFABC.