Renal mitochondrial impairment is attenuated by AT 1 blockade in experimental Type I diabetes
Abstract
To investigate whether ANG II type 1 (AT 1 ) receptor blockade could protect kidney mitochondria in streptozotocin-induced Type 1 diabetes, we treated 8-wk-old male Sprague-Dawley rats with a single streptozotocin injection (65 mg/kg ip; STZ group), streptozotocin and drinking water containing either losartan (30 mg·kg −1 ·day −1 ; STZ+Los group) or amlodipine (3 mg·kg −1 ·day −1 ; STZ+Amlo group), or saline (intraperitoneally) and pure water (control group). Four-month-long losartan or amlodipine treatments started 30 days before streptozotocin injection to improve the antioxidant defenses. The number of renal lesions, plasma glucose and lipid levels, and proteinuria were higher and creatinine clearance was lower in STZ and STZ+Amlo compared with STZ+Los and control groups. Glycemia was higher in STZ+Los compared with control. Blood pressure, basal mitochondrial membrane potential and mitochondrial pyruvate content, and renal oxidized glutathione levels were higher and NADH/cytochrome c oxidoreductase activity was lower in STZ compared with the other groups. In STZ and STZ+Amlo groups, mitochondrial H 2 O 2 production rate was higher and uncoupling protein-2 content, cytochrome c oxidase activity, and renal glutathione level were lower than in STZ+Los and control groups. Mitochondrial nitric oxide synthase activity was higher in STZ+Amlo compared with the other groups. Mitochondrial pyruvate content and H 2 O 2 production rate negatively contributed to electron transfer capacity and positively contributed to renal lesions. Uncoupling protein-2 content negatively contributed to mitochondrial H 2 O 2 production rate and renal lesions. Renal glutathione reduction potential positively contributed to mitochondria electron transfer capacity. In conclusion, AT 1 blockade protects kidney mitochondria and kidney structure in streptozotocin-induced diabetes independently of blood pressure and glycemia.
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UCP2 was negatively associated with H2O2 production in kidney mitochondria of diabetic rats.
“Another report showed that UCP2 was negatively associated with H2O2 production in kidney mitochondria of diabetic rats (79).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [79]
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- Authors
- de Cavanagh, E. M. V., Ferder, L., Toblli, J. E., Piotrkowski, B., Stella, I., Fraga, C. G., & Inserra, F.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2008-01
- Volume
- 294
- Issue
- 1
- Pages
- H456-H465
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2148289342
- Cited by
- 54
- References
- 84
- Citations by year
- 2026: 3 · 2024: 5 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 6 · 2012: 8
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Agencia Nacional de Promoción Científica y Tecnológica
- Comisión de Investigaciones Científicas
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- type 1 diabetes, renal mitochondria, AT1 receptor blockade, losartan, amlodipine, streptozotocin-induced diabetes, mitochondrial dysfunction, oxidative stress, glutathione, UCP2, cytochrome c oxidase, hydrogen peroxide production, nitric oxide synthase, proteinuria, renal protection
- MeSH terms
- Uncoupling Protein 2, Animals, Antihypertensive Agents, Antioxidants, Blood Glucose, Blood Pressure, Electron Transport Complex IV, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 1, Glutathione, Hydrogen Peroxide, Ion Channels, Kidney, Male, Mitochondria, Rats, Sprague-Dawley, Amlodipine, Reactive Oxygen Species, Nitric Oxide Synthase, Pyruvic Acid, Losartan, Mitochondrial Proteins, Receptor, Angiotensin, Type 1, Angiotensin II Type 1 Receptor Blockers, Rats, Membrane Potential, Mitochondrial
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