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

Lu XM, Jin YN, Ma L - Exp Ther Med (2014)

Bottom Line: The results showed that MI induced a reduction in cardiac function and an increase in systolic blood pressure.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

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.

No MeSH data available.


Related in: MedlinePlus

Representative PAS staining results of each group (magnification, ×400). (A) SHAM; (B) MI and (C) OLM group. PAS, periodic acid-Schiff; SHAM, sham surgery; MI, myocardial infarction; OLM, olmesartan medoxomil.
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f1-etm-08-01-0105: Representative PAS staining results of each group (magnification, ×400). (A) SHAM; (B) MI and (C) OLM group. PAS, periodic acid-Schiff; SHAM, sham surgery; MI, myocardial infarction; OLM, olmesartan medoxomil.

Mentions: In the SHAM group, the PAS staining indicated normal glomerular and tubular structures, renal tubular epithelial cells arranged in neat rows and no inflammatory cell infiltration in the stroma. By contrast, in the MI group, glomerular mesangial and tubular lumen expansion and irregular thickening of the basement membrane were observed, and the renal interstitial PAS positive staining was markedly increased compared with that in the SHAM group. These changes were clearly reduced in the OLM group. The results are shown in Fig. 1.


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

Lu XM, Jin YN, Ma L - Exp Ther Med (2014)

Representative PAS staining results of each group (magnification, ×400). (A) SHAM; (B) MI and (C) OLM group. PAS, periodic acid-Schiff; SHAM, sham surgery; MI, myocardial infarction; OLM, olmesartan medoxomil.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061226&req=5

f1-etm-08-01-0105: Representative PAS staining results of each group (magnification, ×400). (A) SHAM; (B) MI and (C) OLM group. PAS, periodic acid-Schiff; SHAM, sham surgery; MI, myocardial infarction; OLM, olmesartan medoxomil.
Mentions: In the SHAM group, the PAS staining indicated normal glomerular and tubular structures, renal tubular epithelial cells arranged in neat rows and no inflammatory cell infiltration in the stroma. By contrast, in the MI group, glomerular mesangial and tubular lumen expansion and irregular thickening of the basement membrane were observed, and the renal interstitial PAS positive staining was markedly increased compared with that in the SHAM group. These changes were clearly reduced in the OLM group. The results are shown in Fig. 1.

Bottom Line: The results showed that MI induced a reduction in cardiac function and an increase in systolic blood pressure.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

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.

No MeSH data available.


Related in: MedlinePlus