ArticleAmerican journal of physiology. Renal physiology2012
Effects of the antioxidant drug tempol on renal oxygenation in mice with reduced renal mass.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Maternal undernourishment impairs murine placental development during pregnancy.BMC pregnancy and childbirth · 2025Article
- Activation of Nrf2 in Mice Causes Early Microvascular Cyclooxygenase-Dependent Oxidative Stress and Enhanced Contractility.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Involvement of Vanin-1 in Ameliorating Effect of Oxidative Renal Tubular Injury in Dahl-Salt Sensitive Rats.International journal of molecular sciences · 2019Article
- High Salt Enhances Reactive Oxygen Species and Angiotensin II Contractions of Glomerular Afferent Arterioles From Mice With Reduced Renal Mass.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Biomarkers for Chronic Kidney Disease Associated with High Salt Intake.International journal of molecular sciences · 2017Review
- Increasing UCP2 expression and decreasing NOX1/4 expression maintain chondrocyte phenotype by reducing reactive oxygen species production.Oncotarget · 2017Article
- Reno-Cerebral Reflex Activates the Renin-Angiotensin System, Promoting Oxidative Stress and Renal Damage After Ischemia-Reperfusion Injury.Antioxidants & redox signaling · 2017Article
- Superoxide and hydrogen peroxide counterregulate myogenic contractions in renal afferent arterioles from a mouse model of chronic kidney disease.Kidney international · 2017Article
- High-salt diet induces outward remodelling of efferent arterioles in mice with reduced renal mass.Acta physiologica (Oxford, England) · 2017Article
- Immunohistochemical expression of intrarenal renin angiotensin system components in response to tempol in rats fed a high salt diet.World journal of nephrology · 2017Article
- Paracellular epithelial sodium transport maximizes energy efficiency in the kidney.The Journal of clinical investigation · 2016Article
- Differential effects of superoxide and hydrogen peroxide on myogenic signaling, membrane potential, and contractions of mouse renal afferent arterioles.American journal of physiology. Renal physiology · 2016Article
- Hyperglycemia Induces Cellular Hypoxia through Production of Mitochondrial ROS Followed by Suppression of Aquaporin-1.PloS one · 2016Article
- Early urinary biomarkers for renal tubular damage in spontaneously hypertensive rats on a high salt intake.Hypertension research : official journal of the Japanese Society of Hypertension · 2016Article
- Protective Effect of Tempol on Acute Kidney Injury Through PI3K/Akt/Nrf2 Signaling Pathway.Kidney & blood pressure research · 2016Article
- A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression.Journal of the American Society of Nephrology : JASN · 2015Article
- Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- High-salt diet blunts renal autoregulation by a reactive oxygen species-dependent mechanism.American journal of physiology. Renal physiology · 2014Article
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15 authors.
Funding
Abstract
We tested the hypothesis that reactive oxygen species (ROS) contributed to renal hypoxia in C57BL/6 mice with ⅚ surgical reduction of renal mass (RRM). ROS can activate the mitochondrial uncoupling protein 2 (UCP-2) and increase O(2) usage. However, UCP-2 can be inactivated by glutathionylation. Mice were fed normal (NS)- or high-salt (HS) diets, and HS mice received the antioxidant drug tempol or vehicle for 3 mo. Since salt intake did not affect the tubular Na(+) transport per O(2) consumed (T(Na/)Q(O2)), further studies were confined to HS mice. RRM mice had increased excretion of 8-isoprostane F(2α) and H(2)O(2), renal expression of UCP-2 and renal O(2) extraction, and reduced T(Na/)Q(O2) (sham: 20 ± 2 vs. RRM: 10 ± 1 μmol/μmol; P < 0.05) and cortical Po(2) (sham: 43 ± 2, RRM: 29 ± 2 mmHg; P < 0.02). Tempol normalized all these parameters while further increasing compensatory renal growth and glomerular volume. RRM mice had preserved blood pressure, glomeruli, and patchy tubulointerstitial fibrosis. The patterns of protein expression in the renal cortex suggested that RRM kidneys had increased ROS from upregulated p22(phox), NOX-2, and -4 and that ROS-dependent increases in UCP-2 led to hypoxia that activated transforming growth factor-β whereas erythroid-related factor 2 (Nrf-2), glutathione peroxidase-1, and glutathione-S-transferase mu-1 were upregulated independently of ROS. We conclude that RRM activated distinct processes: a ROS-dependent activation of UCP-2 leading to inefficient renal O(2) usage and cortical hypoxia that was offset by Nrf-2-dependent glutathionylation. Thus hypoxia in RRM may be the outcome of NADPH oxidase-initiated ROS generation, leading to mitochondrial uncoupling counteracted by defense pathways coordinated by Nrf-2.
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