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Modulation of haemodynamics, endogeneous antioxidant enzymes, and pathophysiological changes by selective inhibition

Ghulam Moinuddin1, Mohammed Naseeruddin Inamdar, Kala S Kulkarni

  • 1Department of Pharmacology, Al-Ameen College of Pharmacy, Bangalore, India. moinuddin5@gmail.com

Cardiovascular Journal of Africa
|June 6, 2013
PubMed

Insights

Angiotensin II receptor blockers improved blood pressure and antioxidant enzyme activity in rats with pressure-overload cardiac hypertrophy. These drugs also protected target organs from hypertension-induced damage.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Nephrology

Background:

  • Constriction of the thoracic or abdominal aorta models pressure-overload cardiac hypertrophy.
  • Blockade of angiotensin II type 1 (AT1) receptors mitigates target-organ damage in hypertension.

Purpose of the Study:

  • To investigate the effects of angiotensin II receptor antagonists on blood pressure.
  • To assess changes in endogenous antioxidant enzymes (catalase and superoxide dismutase).
  • To evaluate histopathological alterations in pressure-overload rat models.

Main Methods:

  • Cardiac hypertrophy was induced in male rats via abdominal aortic banding (AAB).
  • AAB-induced hypertensive rats received losartan, candesartan, or irbesartan for 16 weeks.
  • Measurements included non-invasive blood pressure, antioxidant enzyme activities, and organ histology.

Main Results:

  • AAB induced sustained hypertension and reduced catalase and superoxide dismutase (SOD) activity.
  • AT1 receptor antagonist treatment significantly lowered systolic blood pressure.
  • Treated rats exhibited increased serum SOD and catalase activities and attenuated target organ damage.

Conclusions:

  • AT1 receptor blockade enhances myocardial antioxidant capacity in hypertensive rats.
  • This blockade reduces oxidative stress, as evidenced by organ protection.
  • Angiotensin II receptor antagonists offer a protective effect against pressure-overload-induced organ damage.
Abstract

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