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Modulation of haemodynamics, endogeneous antioxidant enzymes, and pathophysiological changes by selective inhibition of angiotensin II type 1 receptors in pressureoverload rats.

Moinuddin G, Inamdar MN, Kulkarni KS, Kulkarni C - Cardiovasc J Afr (2013)

Bottom Line: Blockade of AT1 receptors is beneficial in preventing target-organ damage in hypertension.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.

View Article: PubMed Central - HTML - PubMed

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

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.

Conclusion: 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.

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Kidney and thoracic aorta sections of normal, hypertensive and AT 1 receptor blocker-treated groups. A: Normal kidney section (4×) B: Hypertensive kidneys showing severe oedema, characterised by dilatation of the tubules and haemorrhage in the glomeruli and tubules (10×); C: Losartan-treated kidneys showing minimal vacuolations (4×); D: Candesartan-treated kidneys showing moderate oedema and haemorrhage, and hypertrophy of the tubules (10×); E: Irbesartan-treated kidneys showing moderate oedema, haemorrhage and hypertrophy of the tubules (10×); F: Normal thoracic aorta sections (4×) G: Hypertensive aorta showing minimal foam cell formation in between the fibres (4×); H: Losartan-treated aorta showing no changes (4×); I: Candesartan-treated aorta showing one or two foam cells (4×); J: Irbesartan-treated aorta showing no changes (4×).
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Figure 2: Kidney and thoracic aorta sections of normal, hypertensive and AT 1 receptor blocker-treated groups. A: Normal kidney section (4×) B: Hypertensive kidneys showing severe oedema, characterised by dilatation of the tubules and haemorrhage in the glomeruli and tubules (10×); C: Losartan-treated kidneys showing minimal vacuolations (4×); D: Candesartan-treated kidneys showing moderate oedema and haemorrhage, and hypertrophy of the tubules (10×); E: Irbesartan-treated kidneys showing moderate oedema, haemorrhage and hypertrophy of the tubules (10×); F: Normal thoracic aorta sections (4×) G: Hypertensive aorta showing minimal foam cell formation in between the fibres (4×); H: Losartan-treated aorta showing no changes (4×); I: Candesartan-treated aorta showing one or two foam cells (4×); J: Irbesartan-treated aorta showing no changes (4×).

Mentions: The sections of normal control, sham-operated rat kidneys showed normal structure and architecture. The kidney section of the untreated AABIH rats showed oedema, vacuolations in the tubules, moderate to severe haemorrhage and congested vessels. Compared to the untreated AABIH group, the kidney sections of the losartan-treated group showed oedema, vacuolations in the tubules, a moderate degree of haemorrhage, congested blood vessels, and dilatation of vessels and hypertrophy of the tubules. The sections of the candesartan-treated group showed mild oedema, vacuolations in the tubules, a mild-to-moderate degree of haemorrhage, and congested blood vessels. The sections of the irbesartan-treated group showed mild oedema, vacuolations in the tubules, a mild-to-moderate degree of haemorrhage, and congested blood vessels (Fig. 2A - E).


Modulation of haemodynamics, endogeneous antioxidant enzymes, and pathophysiological changes by selective inhibition of angiotensin II type 1 receptors in pressureoverload rats.

Moinuddin G, Inamdar MN, Kulkarni KS, Kulkarni C - Cardiovasc J Afr (2013)

Kidney and thoracic aorta sections of normal, hypertensive and AT 1 receptor blocker-treated groups. A: Normal kidney section (4×) B: Hypertensive kidneys showing severe oedema, characterised by dilatation of the tubules and haemorrhage in the glomeruli and tubules (10×); C: Losartan-treated kidneys showing minimal vacuolations (4×); D: Candesartan-treated kidneys showing moderate oedema and haemorrhage, and hypertrophy of the tubules (10×); E: Irbesartan-treated kidneys showing moderate oedema, haemorrhage and hypertrophy of the tubules (10×); F: Normal thoracic aorta sections (4×) G: Hypertensive aorta showing minimal foam cell formation in between the fibres (4×); H: Losartan-treated aorta showing no changes (4×); I: Candesartan-treated aorta showing one or two foam cells (4×); J: Irbesartan-treated aorta showing no changes (4×).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3721829&req=5

Figure 2: Kidney and thoracic aorta sections of normal, hypertensive and AT 1 receptor blocker-treated groups. A: Normal kidney section (4×) B: Hypertensive kidneys showing severe oedema, characterised by dilatation of the tubules and haemorrhage in the glomeruli and tubules (10×); C: Losartan-treated kidneys showing minimal vacuolations (4×); D: Candesartan-treated kidneys showing moderate oedema and haemorrhage, and hypertrophy of the tubules (10×); E: Irbesartan-treated kidneys showing moderate oedema, haemorrhage and hypertrophy of the tubules (10×); F: Normal thoracic aorta sections (4×) G: Hypertensive aorta showing minimal foam cell formation in between the fibres (4×); H: Losartan-treated aorta showing no changes (4×); I: Candesartan-treated aorta showing one or two foam cells (4×); J: Irbesartan-treated aorta showing no changes (4×).
Mentions: The sections of normal control, sham-operated rat kidneys showed normal structure and architecture. The kidney section of the untreated AABIH rats showed oedema, vacuolations in the tubules, moderate to severe haemorrhage and congested vessels. Compared to the untreated AABIH group, the kidney sections of the losartan-treated group showed oedema, vacuolations in the tubules, a moderate degree of haemorrhage, congested blood vessels, and dilatation of vessels and hypertrophy of the tubules. The sections of the candesartan-treated group showed mild oedema, vacuolations in the tubules, a mild-to-moderate degree of haemorrhage, and congested blood vessels. The sections of the irbesartan-treated group showed mild oedema, vacuolations in the tubules, a mild-to-moderate degree of haemorrhage, and congested blood vessels (Fig. 2A - E).

Bottom Line: Blockade of AT1 receptors is beneficial in preventing target-organ damage in hypertension.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.

View Article: PubMed Central - HTML - PubMed

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

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.

Conclusion: 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.

Show MeSH
Related in: MedlinePlus