Manifestation of Oxidative Stress in the Pathogenesis of Arterial Hypertension in ISIAH Rats

Yelinova, V.I.; Khramtsov, Valery V.; Al, Markel'

doi:10.1006/bbrc.1999.1396

Cited by 17 publications

(11 citation statements)

References 11 publications

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“…Alternative agents with SOD-like activity have been investigated, and among these, Tempol demonstrates attenuation of hypertension30. Along this line, low activity of SOD renal was observed in FS rats and low levels of SOD are present in IR and in hypertension in humans studies and experimental animals313233. We provided strong functional data to support involvement of a possibly inefficient antioxidant system causing hypertension.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress causes hypertension and activation of nuclear factor-κB after high-fructose and salt treatments

Dornas

Cardoso

Silva

et al. 2017

Sci Rep

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There is evidence that diets rich in salt or simple sugars as fructose are associated with abnormalities in blood pressure regulation. However, the mechanisms underlying pathogenesis of salt- and fructose-induced kidney damage and/or consequent hypertension yet remain largely unexplored. Here, we tested the role of oxidative state as an essential factor along with high salt and fructose treatment in causing hypertension. Fischer male rats were supplemented with a high-fructose diet (20% in water) for 20 weeks and maintained on high-salt diet (8%) associate in the last 10 weeks. Fructose-fed rats exhibited a salt-dependent hypertension accompanied by decrease in renal superoxide dismutase activity, which is the first footprint of antioxidant inactivation by reactive oxygen species (ROS). Metabolic changes and the hypertensive effect of the combined fructose-salt diet (20 weeks) were markedly reversed by a superoxide scavenger, Tempol (10 mg/kg, gavage); moreover, Tempol (50 mM) potentially reduced ROS production and abolished nuclear factor-kappa B (NF-κB) activation in human embryonic kidney HEK293 cells incubated with L-fructose (30 mM) and NaCl (500 mosmol/kg added). Taken together, our data suggested a possible role of oxygen radicals and ROS-induced activation of NF-κB in the fructose- and salt-induced hypertension associated with the progression of the renal disease.

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Section: Discussionmentioning

confidence: 99%

Oxidative stress causes hypertension and activation of nuclear factor-κB after high-fructose and salt treatments

Dornas

Cardoso

Silva

et al. 2017

Sci Rep

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“…The findings suggest that oxidative stress may play a significant role in the pathogenesis of stress-sensitive hypertension in this rat strain resulting, in part, in an increased level of GSH oxidation (118).…”

Section: Noninvasive Measurement Of Thiols Using Disulfide R 2 Ssr 2 mentioning

confidence: 82%

“…Low nontoxic concentrations of the label R 2 SSR 2 were used to measure thiols in rat blood, demonstrating an increased depletion of GSH in an animal model of stress-sensitive arterial hypertension (118). The findings suggest that oxidative stress may play a significant role in the pathogenesis of stress-sensitive hypertension in this rat strain resulting, in part, in an increased level of GSH oxidation (118).…”

Section: Noninvasive Measurement Of Thiols Using Disulfide R 2 Ssr 2 mentioning

confidence: 96%

Use of Electron Paramagnetic Resonance Spectroscopy to Evaluate the Redox StateIn Vivo

Swartz

Khan

Khramtsov

2007

Antioxidants & Redox Signaling

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The aim of this article is to provide an overview of how electron paramagnetic resonance (EPR) can be used to measure redox-related parameters in vivo. The values of this approach include that the measurements are made under fully physiological conditions, and some of the measurements cannot be made by other means. Three complementary approaches are used with in vivo EPR: the rate of reduction or reactions of nitroxides, spin trapping of free radicals, and measurements of thiols. All three approaches already have produced unique and useful information. The measurement of the rate of decrease of nitroxides technically is the simplest, but difficult to interpret because the measured parameter, reduction in the intensity of the nitroxide signal, can occur by several different mechanisms. In vivo spin trapping can provide direct evidence for the occurrence of specific free radicals in vivo and reflect relative changes, but accurate absolute quantification remains challenging. The measurement of thiols in vivo also appears likely to be useful, but its development as an in vivo technique is at an early stage. It seems likely that the use of in vivo EPR to measure redox processes will become an increasingly utilized and valuable tool. OVERVIEWThe goal of this article is to indicate how the unique capabilities of EPR can be used very effectively to follow redox status/events in vivo. This will be done in the context of a general overview and two more detailed complementary mini-reviews of the current status of the use of in vivo EPR to measure free radicals and thiols. The article also seeks to delineate areas where developments are needed and the potential pathways to achieve them.The ability to measure redox status and redox processes in vivo is very attractive for several reasons. It has been clearly established that redox-active species are intrinsically involved in many physiological and pathophysiological processes. The roles of these species include being essential intermediates in key physiological reactions and, in many cases, being directly involved in the causal chain leading to pathology. The redox state is an important parameter for many key events in cell signaling (13). Also, therapeutic approaches for many types of pathophysiology involve redox reactions (84).Whereas many useful insights can be achieved by measurements in model systems and cell cultures, the complexity of redox processes and physiology makes it difficult to understand fully the redox processes that occur in vivo without making direct measurements with the intact NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript system. The dynamics of the vascular system, metabolism in different organs, and the complex web of oxidants and antioxidants, cannot be modeled readily. There are few techniques that are capable of making such measurements in vivo, but fortunately EPR can follow many of the most important aspects of these complex processes.Some of the redox-active species are free radicals, and for these, EPR is t...

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“…Recent findings suggest that the interactions with superoxide radicals, thiols, and metals, particularly with Fe 2ϩ , may be important in channeling NO from physiologically to pathophysiologically relevant effects (24 -26). Thus, enhanced levels of NO-derived oxidants (e.g., peroxynitirite) appear to mediate endothelium damaging effects in various disorders (e.g., stroke and myocardial infarction) and have also been suggested to play a pathogenic role in the development of hypertension in animal models (23,27). Therefore, rather than being protective, enhanced NO production may, through increased oxidative stress and endothelial damaging mechanisms, mediate harmful effects in HTx recipients.…”

Section: Discussionmentioning

confidence: 99%

Hypertension in relation to nitric oxide, asymmetric dimethylarginine, and inflammation: different patterns in heart transplant recipients and individuals with essential hypertension

Holm

Aukrust²,

Aagaard³

et al. 2002

Transplantation

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Manifestation of Oxidative Stress in the Pathogenesis of Arterial Hypertension in ISIAH Rats

Cited by 17 publications

References 11 publications

Oxidative stress causes hypertension and activation of nuclear factor-κB after high-fructose and salt treatments

Oxidative stress causes hypertension and activation of nuclear factor-κB after high-fructose and salt treatments

Use of Electron Paramagnetic Resonance Spectroscopy to Evaluate the Redox StateIn Vivo

Hypertension in relation to nitric oxide, asymmetric dimethylarginine, and inflammation: different patterns in heart transplant recipients and individuals with essential hypertension

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