title: Modulation of haemodynamics, endogeneous antioxidant enzymes, and pathophysiological changes by selective inhibition of angiotensin II type 1 receptors in pressureoverload rats.
abstract: BACKGROUND
  Constriction of the thoracic or abdominal aorta provides an experimental model of pressure-overload cardiac hypertrophy. Blockade of AT1 receptors is beneficial in preventing target-organ damage in hypertension.
  
  
  OBJECTIVE
  To examine the effect of angiotensin II receptor antagonists on blood pressure, endogenous antioxidant enzyme and histopathological changes in pressure-overload rats.
  
  
  METHODS
  Pressure overload was produced by abdominal aortic banding (AAB) using a blunt 22-guage needle in male rats as a model of cardiac hypertrophy. After surgery, the AAB-induced hypertension (AABIH) rats were treated with losartan 40 mg/kg/day, candesartan 10 mg/kg/day, irbesartan 10 mg/kg/day per os for 16 weeks. At 16 weeks of surgery, the rats were observed for general characteristics and mortality, and we determined non-invasive blood pressure (NIBP), endogenous antioxidant enzyme catalase and superoxide dismutase (SOD) activities, and histology of the target organs.
  
  
  RESULTS
  In the AABIH group, significant increase in systolic blood pressure was observed from weeks 3 to 16 compared with the control group, along with reduced serum catalase and SOD activities. The treated groups showed significant reduction in systolic BP and increase in serum SOD and catalase activities. The histological changes induced in the target organs, namely heart, liver, kidneys and thoracic aorta in the AABIH rats were attenuated in the treated rats.
  
  
  CONCLUSIONS
  Blockade of the AT1 receptor caused an improvement in the myocardial antioxidant reserve and decreased oxidative stress in the hypertensive rats, which was evidenced by the protection observed in the treatment groups.
authors.affiliation: Department of Pharmacology, Al-Ameen College of Pharmacy, Bangalore, India. moinuddin5@gmail.com
authors.forename: Ghulam
authors.initials: G
authors.lastname: Moinuddin
authors.forename: Mohammed Naseeruddin
authors.initials: MN
authors.lastname: Inamdar
authors.forename: Kala S
authors.initials: KS
authors.lastname: Kulkarni
authors.forename: Chanda
authors.initials: C
authors.lastname: Kulkarni
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D006332:Cardiomegaly / Q000201:enzymology / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D002374:Catalase / Q000378:metabolism*; D004195:Disease Models, Animal; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D000077405:Irbesartan; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism*; D013777:Tetrazoles / Q000494:pharmacology; D013997:Time Factors
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000975:Antioxidants; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; D002374:Catalase; D013482:Superoxide Dismutase; D000077405:Irbesartan; D019808:Losartan; C081643:candesartan