Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension
Joint Authors
Zazueta, Cecilia
Johnson, Richard J.
García-Arroyo, Fernando Enrique
Cristóbal-García, Magdalena
Sánchez-Lozada, Laura Gabriela
Madero, Magdalena
Rodríguez-Iturbe, Bernardo
Correa, Francisco
Tapia, Edilia
Pedraza-Chaverri, José
Arellano, Abraham
Osorio, Horacio
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-8, 8 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-03-31
Country of Publication
Egypt
No. of Pages
8
Main Subjects
Abstract EN
We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia.
A second objective was to evaluate whether the long-term treatment with the antioxidant Tempol prevents renal oxidative stress, mitochondrial alterations, and systemic hypertension in this model.
Long-term (11-12 weeks) and short-term (3 weeks) effects of oxonic acid induced hyperuricemia were studied in rats (OA, 750 mg/kg BW), OA+Allopurinol (AP, 150 mg/L drinking water), OA+Tempol (T, 15 mg/kg BW), or vehicle.
Systolic blood pressure, renal blood flow, and vascular resistance were measured.
Tubular damage (urine N-acetyl-β-D-glucosaminidase) and oxidative stress markers (lipid and protein oxidation) along with ATP levels were determined in kidney tissue.
Oxygen consumption, aconitase activity, and uric acid were evaluated in isolated mitochondria from renal cortex.
Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction.
Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels.
Treatments with Tempol and allopurinol prevented these alterations.
Renal oxidative stress induced by hyperuricemia promoted mitochondrial functional disturbances and decreased ATP content, which represent an additional pathogenic mechanism induced by chronic hyperuricemia.
Hyperuricemia-related hypertension occurs before these changes are evident.
American Psychological Association (APA)
Cristóbal-García, Magdalena& García-Arroyo, Fernando Enrique& Tapia, Edilia& Osorio, Horacio& Arellano, Abraham& Madero, Magdalena…[et al.]. 2015. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
Modern Language Association (MLA)
Cristóbal-García, Magdalena…[et al.]. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity No. 2015 (2015), pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
American Medical Association (AMA)
Cristóbal-García, Magdalena& García-Arroyo, Fernando Enrique& Tapia, Edilia& Osorio, Horacio& Arellano, Abraham& Madero, Magdalena…[et al.]. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity. 2015. Vol. 2015, no. 2015, pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1075685