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

Xiao-Mei Lu1, Yu-Nan Jin1, Ling Ma1

  • 1Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

Experimental and Therapeutic Medicine
|June 20, 2014
PubMed

Insights

Myocardial infarction (MI) activates the kidney

Area of Science:

  • Cardiovascular Research
  • Nephrology
  • Pharmacology

Background:

  • Myocardial infarction (MI) can lead to secondary organ damage.
  • The intrarenal renin-angiotensin system (RAS) plays a role in kidney injury.
  • Olmesartan medoxomil (OLM) is an angiotensin II receptor blocker.

Purpose of the Study:

  • To investigate the protective effects of olmesartan medoxomil (OLM) against renal injury following myocardial infarction (MI) in a mouse model.
  • To elucidate the mechanisms by which OLM influences the intrarenal RAS and renal pathology.

Main Methods:

  • Establishment of experimental myocardial infarction (MI) in male C57/BL/6 mice via coronary artery ligation.
  • Administration of olmesartan medoxomil (OLM) at 10 mg/kg daily for eight weeks in the treatment group.
  • Assessment of cardiac function, systolic blood pressure, renal histology (PAS staining), and intrarenal/plasma levels of angiotensin II (Ang II), renin, angiotensin II type 1 receptor (AT1R), and angiotensinogen (AGT).

Main Results:

  • MI induced cardiac dysfunction, increased systolic blood pressure, and significant renal injury evidenced by PAS staining.
  • MI elevated plasma and kidney Ang II levels, alongside increased renal expression of renin, AT1R, and AGT.
  • OLM treatment significantly reduced systolic blood pressure, attenuated renal injury, and decreased Ang II, renin, AT1R, and AGT levels compared to the MI group.

Conclusions:

  • Myocardial infarction (MI) activates the intrarenal renin-angiotensin system (RAS), contributing to glomerulosclerosis.
  • Olmesartan medoxomil (OLM) demonstrates renoprotective effects post-MI by inhibiting the intrarenal RAS and mitigating Ang II-mediated damage.
Keywords:
mousemyocardial infarctionolmesartan medoxomil

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