ArticleAmerican journal of physiology. Heart and circulatory physiology2008
NAD(P)H oxidase-derived peroxide mediates elevated basal and impaired flow-induced NO production in SHR mesenteric arteries in vivo.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
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- Combination of Exercise Training and SOD Mimetic Tempol Enhances Upregulation of Nitric Oxide Synthase in the Kidney of Spontaneously Hypertensive Rats.International journal of hypertension · 2020Article
- Oxidative Stress and Hypertensive Diseases.The Medical clinics of North America · 2017Review
- The Pathophysiological Role of NOX2 in Hypertension and Organ Damage.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2016Review
- Role of MicroRNA in Endothelial Dysfunction and Hypertension.Current hypertension reports · 2016Review
- Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus.Cardiovascular diabetology · 2016Article
- Resveratrol Improved Flow-Mediated Outward Arterial Remodeling in Ovariectomized Rats with Hypertrophic Effect at High Dose.PloS one · 2016Article
- Modeling Disease Progression: Angiotensin II Indirectly Inhibits Nitric Oxide Production via ADMA Accumulation in Spontaneously Hypertensive Rats.Frontiers in physiology · 2016Article
- Impaired compensation to femoral artery ligation in diet-induced obese mice is primarily mediated via suppression of collateral growth by Nox2 and p47phox.American journal of physiology. Heart and circulatory physiology · 2015Article
- Evolution of NADPH Oxidase Inhibitors: Selectivity and Mechanisms for Target Engagement.Antioxidants & redox signaling · 2015Review
- Effect of Selenium Supplementation on Redox Status of the Aortic Wall in Young Spontaneously Hypertensive Rats.Oxidative medicine and cellular longevity · 2015Article
- Nox2 and p47(phox) modulate compensatory growth of primary collateral arteries.American journal of physiology. Heart and circulatory physiology · 2014Article
- Time-related alteration in flow- (shear stress-) mediated remodeling in resistance arteries from spontaneously hypertensive rats.International journal of hypertension · 2014Article
- Molecular basis for impaired collateral artery growth in the spontaneously hypertensive rat: insight from microarray analysis.Physiological reports · 2013Article
- Is the real in vivo nitric oxide concentration pico or nano molar? Influence of electrode size on unstirred layers and NO consumption.Microcirculation (New York, N.Y. : 1994) · 2013Article
- Constitutive NADPH oxidase 4 activity resides in the composition of the B-loop and the penultimate C terminus.The Journal of biological chemistry · 2012Article
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- Contribution of oxidative stress to endothelial dysfunction in hypertension.Frontiers in physiology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) and reactive oxygen species (ROS) have fundamentally important roles in the regulation of vascular tone and remodeling. Although arterial disease and endothelial dysfunction alter NO and ROS levels to impact vasodilation and vascular structure, direct measurements of these reactive species under in vivo conditions with flow alterations are unavailable. In this study, in vivo measurements of NO and H2O2 were made on mesenteric arteries to determine whether antioxidant therapies could restore normal NO production in spontaneously hypertensive rats (SHR). Flow was altered from approximately 50-200% of control in anesthetized Wistar-Kyoto rats (WKY) and SHR by selective placement of microvascular clamps on adjacent arteries while NO and H2O2 were directly measured with microelectrodes. Relative to WKY, SHR had significantly increased baseline NO and H2O2 concentrations (2,572 +/- 241 vs. 1,059 +/- 160 nM, P < 0.01; and 26 +/- 7 vs. 7 +/- 1 microM, P < 0.05, respectively). With flow elevation, H2O2 but not NO increased in SHR; NO but not H2O2 was elevated in WKY. Apocynin and polyethylene-glycolated catalase decreased baseline SHR NO and H2O2 to WKY levels and restored flow-mediated NO production. Suppression of NAD(P)H oxidase with gp91ds-tat decreased SHR H2O2 to WKY levels. Addition of topical H2O2 to increase peroxide to the basal concentration measured in SHR elevated WKY NO to levels observed in SHR. The results support the hypothesis that increased vascular peroxide in SHR is primarily derived from NAD(P)H oxidase and increases NO concentration to levels that cannot be further elevated with increased flow. Short-term and even acute administration of antioxidants are able to restore normal flow-mediated NO signaling in young SHR.
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