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Published on: June 29, 2014
Angiotensin II blockade improves mitochondrial function in spontaneously hypertensive rats
E M V De Cavanagh1, J E Toblli, L Ferder
1University of Buenos Aires Physical Chemistry, School of Pharmacy and Biochemistry Junin 956, Buenos Aires (1113), Argentina.
Hypertension damages kidney mitochondria, increasing oxidant production. Candesartan treatment improved mitochondrial function in hypertensive rats, suggesting a mechanism for its renal protective effects.
Area of Science:
- Nephrology
- Cardiovascular Research
- Mitochondrial Biology
Background:
- Hypertension is linked to mitochondrial dysfunction in multiple organs.
- Angiotensin II contributes to oxidant stress and vascular damage.
- Kidney mitochondrial health is crucial for renal function.
Purpose of the Study:
- To determine if hypertension causes kidney mitochondrial dysfunction.
- To investigate if angiotensin II blockade reverses these mitochondrial changes.
- To explore the role of mitochondrial function in candesartan's renal protective effects.
Main Methods:
- Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were used.
- SHR received candesartan (angiotensin II receptor blocker) for 4 months.
- Kidney mitochondrial function, oxidant production, and markers of renal damage were assessed.
Main Results:
- Hypertensive rats exhibited impaired kidney mitochondrial function, reduced enzyme activities, and increased oxidant production.
- Candesartan treatment normalized blood pressure, proteinuria, and preserved kidney mitochondrial function in SHR.
- SHR showed higher glomerular and tubulointerstitial alpha-smooth muscle actin labeling compared to controls and treated rats.
Conclusions:
- Hypertension-induced kidney mitochondrial dysfunction is associated with increased oxidant production.
- Angiotensin II blockade with candesartan preserves kidney mitochondrial function in hypertension.
- Improved mitochondrial function may contribute to the renal protective benefits of candesartan in hypertensive individuals.
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