ArticleThe Journal of biological chemistry2010
Angiotensin II stimulates thick ascending limb superoxide production via protein kinase C(α)-dependent NADPH oxidase activation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Angiotensin II-stimulated proximal nephron superoxide production and fructose-induced salt-sensitive hypertension.American journal of physiology. Renal physiology · 2024Article
- Mechanisms of decreased tubular flow-induced nitric oxide in Dahl salt-sensitive rat thick ascending limbs.American journal of physiology. Renal physiology · 2021Article
- Angiotensin II-induced superoxide and decreased glutathione in proximal tubules: effect of dietary fructose.American journal of physiology. Renal physiology · 2020Article
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- Superoxide increases surface NKCC2 in the rat thick ascending limbs via PKC.American journal of physiology. Renal physiology · 2019Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Angiotensin II Stimulates the NLRP3 Inflammasome to Induce Podocyte Injury and Mitochondrial Dysfunction.Kidney diseases (Basel, Switzerland) · 2018Article
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
- Effects of Reactive Oxygen Species on Tubular Transport along the Nephron.Antioxidants (Basel, Switzerland) · 2017Review
- Brain Renin-Angiotensin System and Microglial Polarization: Implications for Aging and Neurodegeneration.Frontiers in aging neuroscience · 2017Review
- Organic compounds present in airborne particles stimulate superoxide production and DNA fragmentation: role of NOX and xanthine oxidase in animal tissues.Environmental science and pollution research international · 2016Article
- Phytanic acid activates NADPH oxidase through transactivation of epidermal growth factor receptor in vascular smooth muscle cells.Lipids in health and disease · 2016Article
- Angiotensin II stimulates superoxide production by nitric oxide synthase in thick ascending limbs.Physiological reports · 2016Article
- Polydatin Attenuates H2O2-Induced Oxidative Stress via PKC Pathway.Oxidative medicine and cellular longevity · 2016Article
- Lipid-induced NOX2 activation inhibits autophagic flux by impairing lysosomal enzyme activity.Journal of lipid research · 2015Article
- Angiotensin II-induced hypertension blunts thick ascending limb NO production by reducing NO synthase 3 expression and enhancing threonine 495 phosphorylation.American journal of physiology. Renal physiology · 2015Article
- Receptor for advanced glycation end-products regulates lung fluid balance via protein kinase C-gp91(phox) signaling to epithelial sodium channels.American journal of respiratory cell and molecular biology · 2015Article
- Tumor necrosis factor-α: regulation of renal function and blood pressure.American journal of physiology. Renal physiology · 2013Review
- A modern understanding of the traditional and nontraditional biological functions of angiotensin-converting enzyme.Pharmacological reviews · 2013Review
- Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4.American journal of physiology. Cell physiology · 2012Article
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3 authors at 1 institution in 1 country.
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Abstract
Angiotensin II (Ang II) stimulates thick ascending limb (TAL) O₂ production, but the receptor(s) and signaling mechanism(s)involved are unknown. The effect of Ang II on O₂. is generally attributed to the AT₁receptor. In some cells, Ang II stimulates protein kinase C (PKC), whose α isoform (PKCα) can activate NADPH oxidase. We hypothesized that in TALs, Ang II stimulates O₂. via AT₁and PKC α-dependent NADPH oxidase activation.In rat TALs, 1 nM Ang II stimulated O₂. from 0.760.17 to 1.97 0.21 nmol/min/mg (p < 0.001). An AT₁antagonist blocked the stimulatory effect of Ang II on O₂. (0.87 0.25 nmol/min/mg; p < 0.006), whereas an AT₂ antagonist had no effect (2.16 0.133 nmol/min/mg; p < 0.05 versus vehicle). Apocynin, an NADPH oxidase inhibitor, blocked Ang II-stimulated O₂by 90% (p <0.01). Ang II failed to stimulate O₂. in TALs from p47(phox) -/- mice (p < 0.02). Monitored by fluorescence resonance energy transfer, Ang II increased PKC activity from 0.02 0.03 to 0.13 0.02 arbitrary units (p < 0.03). A general PKC inhibitor, GF109203X, blocked the effect of Ang II on O₂(1.47 +/- .21 versus 2.72 +/- .47 nmol/min/mg with Ang II alone; p < 0.03). A PKCα- and ß-selective inhibitor, Gö6976, also blocked the stimulatory effect of Ang II on O₂. (0.59 +/- 0.15 versus 2.05 +/- 0.28 nmol/min/mg with Ang II alone; p < 0.001). To distinguish between PKC α and PKC ß, we used tubules expressing dominant-negative PKC α or -ß. In control TALs, Ang II stimulated O2. by 2.17 0.44 nmol/min/mg (p < 0.011). In tubules expressing dominant-negative PKC α, Ang II failed to stimulate O2. (change: -0.30 +/- 0.27 nmol/min/mg). In tubules expressing dominant-negative PKC ß1, Ang II stimulated O2. by 2.080.69 nmol/min/mg (p < 0.002). We conclude that Ang II stimulates TAL O₂production via activation of AT₁receptors and PKC α-dependent NADPH oxidase.
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