Oxidative Stress in the Sympathetic Premotor Neurons Contributes to Sympathetic Activation in Renovascular Hypertension

Oliveira‐Sales, Elizabeth Barbosa; Nishi, Érika E.; Carillo, Bruno A.; Boim, Mirian Aparecida; Dolnikoff, Miriam Sterman; Bergamaschi, Cássia T.; Campos, Rui

doi:10.1038/ajh.2009.17

Cited by 135 publications

(138 citation statements)

References 34 publications

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“…In the previous study, we observed an imbalance of the autonomic control of the cardiovascular system (sympathetic overactivity and impaired parasympathetic activity) in the 2K1C model of renovascular hypertension . Moreover, augmented ROS production mediates the Ang II actions and results in a sympathetic tone imbalance (Zimmerman et al, 2004;Gao et al, 2005;Oliveira-Sales et al, 2009), which worsens cardiovascular disease processes (Abboud, 2010;Campos et al, 2011). Additionally, in models of infused or endogenous (2K1C) Ang II, inhibition of ROS partly attenuates hypertension, indicating that Ang II-induced ROS is important for vasoconstriction in these models (Taniyama and Griendling, 2003).…”

Section: K1c Hypertension Affects Bone Marrow Cellsmentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.

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Section: K1c Hypertension Affects Bone Marrow Cellsmentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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“…64 The paraventricular nucleus of the hypothalamus is most likely also involved in the ROS-mediated neural mechanism of hypertension. 60,66 There is evidence that other regions of the brain are likewise involved in ROSmediated hypertension. These investigations suggest that increased intracellular superoxide production in the subfornical organ is critical to the development of AT-II-induced hypertension.…”

Section: Urotensin-iimentioning

confidence: 99%

The role of oxidative stress in the pathophysiology of hypertension

2011

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Hypertension is considered to be the most important risk factor in the development of cardiovascular disease. An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. The bioavailability of nitric oxide (NO), which is a major vasodilator, is highly dependent on the redox status. Under physiological conditions, low concentrations of intracellular ROS have an important role in the normal redox signaling maintaining vascular function and integrity. However, under pathophysiological conditions, increased levels of ROS contribute to vascular dysfunction and remodeling through oxidative damage. In human hypertension, an increase in the production of superoxide anions and hydrogen peroxide, a decrease in NO synthesis and a reduction in antioxidant bioavailability have been observed. In turn, antioxidants are reducing agents that can neutralize these oxidative and otherwise damaging biomolecules. The use of antioxidant vitamins, such as vitamins C and E, has gained considerable interest as protecting agents against vascular endothelial damage. Available data support the role of these vitamins as effective antioxidants that can counteract ROS effects. This review discusses the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of vascular damage in hypertension, and the possible therapeutic strategies that could prevent or treat this disorder. Hypertension Research (2011) 34, 431-440; doi:10.1038/hr.2010.264; published online 13 January 2011Keywords: antioxidants; endothelial dysfunction; oxidative stress INTRODUCTION Hypertension is considered the most important risk factor for the occurrence of cardiovascular disease. 1 Oxidative stress has gained attention as one of the fundamental mechanisms responsible for the development of hypertension. Reactive oxygen species (ROS) have an important role in the homeostasis of the vascular wall; hence, they could be part of the mechanism that leads to hypertension. 2-4 Thus, increased ROS production, reduced nitric oxide (NO) levels and reduced antioxidant bioavailability were demonstrated in experimental and human hypertension. Vascular superoxide is primarily derived from nicotinamide adenine dineucleotide phosphate (NADPH) oxidase when stimulated by hormones, such as angiotensin II (AT-II), endothelin-1 (ET-1) and urotensin II. In addition, increased ROS production may be generated by mechanical stimuli on the vascular wall, which increase with hypertension. ROS-induced vasoconstriction results from increased intracellular calcium concentration, thereby contributing to the pathogenesis of hypertension. 2 Vasomotor tone is dependent on a delicate balance between vasoconstrictor and vasodilator forces that result from the interaction between the components of...

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“…Regarding reactive oxygen species in the RVLM, our laboratory and others have shown that Ang II-derived superoxide anions accumulation in the RVLM is critical for the pathogenesis of neurogenic hypertension (Figure 1) [12,17,18,[30][31][32]. The increase of superoxide anions leads to changes in ion channels, particularly calcium and potassium channels, altering neuronal properties in RVLM resulting in increase in sympathetic nerve activity and increase in blood pressure [33].…”

Section: Reactive Oxygen Species In the Rostral Ventrolateral Medullamentioning

confidence: 99%

“…Moreover, adenoviral vectors encoding small interfering RNA to selectively silence Nox2 or Nox4 (two isoforms of the NADPH oxidase) expression in the subfornical organ demonstrate that both Nox2 and Nox4 are required for the full vasopressor effects of brain Ang II [17,18]. One possible downstream mechanism of the activation of AT1R in the SFO and subsequent production of ROS is the superoxide-mediated intracellular calcium influx observed in neuroblastoma Neuro-2A cells, which is inhibited by the adenoviral-mediated expression of a dominant-negative isoform of Rac1 (AdN17Rac1), a critical component for NADPH oxidase activation and superoxide production.…”

Section: Introductionmentioning

confidence: 99%

Brain Angiotensin-II-derived Reactive Oxygen Species: Implications for High Blood Pressure

Carvalho¹,

Guimarães²,

Dantas³

et al. 2012

J Hypertens

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Oxidative Stress in the Sympathetic Premotor Neurons Contributes to Sympathetic Activation in Renovascular Hypertension

Abstract: The data suggest that the hypertension and sympathoexcitation in 2K-1C rats were associated with an increase in oxidative stress within the RVLM, the PVN and systemically.

Cited by 135 publications

References 34 publications

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

The role of oxidative stress in the pathophysiology of hypertension

Brain Angiotensin-II-derived Reactive Oxygen Species: Implications for High Blood Pressure

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