Olmesartan medoxomil reverses glomerulosclerosis in renal tissue induced by myocardial infarction without changes in renal function

Lu,Xiao‑Mei; Jin,Yu‑Nan; Ma,Ling

doi:10.3892/etm.2014.1695

Olmesartan medoxomil reverses glomerulosclerosis in renal tissue induced by myocardial infarction without changes in renal function

Authors:
- Xiao‑Mei Lu
- Yu‑Nan Jin
- Ling Ma
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Affiliations: Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China, Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China
Published online on: April 25, 2014 https://doi.org/10.3892/etm.2014.1695
Pages: 105-109

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Abstract

The aim of the present study was to investigate the effect of olmesartan medoxomil (OLM) on renal injury in mice with myocardial infarction (MI). A total of 33 male C57/BL/6 mice were divided into a sham surgery group (SHAM group), MI group (MI group) and OLM treatment group (OLM group). Experimental MI models were established in the mice of the MI and OLM groups by coronary artery ligation, and the mice in the OLM group were fed a daily dose of 10 mg/kg OLM for eight weeks. The results showed that MI induced a reduction in cardiac function and an increase in systolic blood pressure. In addition, increased periodic acid‑Schiff (PAS) positive staining, combined with increased levels of angiotensin Ⅱ (Ang II) in the plasma and kidneys, and increased expression levels of renin, angiotensin II type 1 receptor (AT1R) and angiotensinogen (AGT) in the kidney tissues was observed compared with those in the SHAM group. OLM treatment attenuated the injury by reducing the systolic blood pressure and PAS positive staining, and decreasing the expression levels of Ang II, renin, AT1R and AGT in the kidney compared with those in the MI group. It may be concluded that MI activates the intrarenal renin‑angiotensin system and leads to glomerulosclerosis, and that OLM protects the kidney by inhibiting the effects of Ang II.

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