Enhanced activation of the respiratory burst oxidase in neutrophils from hypertensive patients

Pontremoli, S.; Salamino, Franca; Sparatore, Bianca; Tullio, Roberta De; Patrone, Mauro; Tizianello, A; Melloni, Edon

doi:10.1016/0006-291x(89)92816-7

Cited by 41 publications

(20 citation statements)

References 12 publications

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“…The results here reported are consistent with the previous finding of abnormally high levels of NADPH oxidase in the course of activation of neutrophils from patients with hypertension, 16 though other authors have found no alteration in the activation pattern of this enzyme in this condition. 17,18 It is noteworthy that Ang II triggers more potent and sustained O 2 Ϫ and ROS production in vitro in human neutrophils than that elicited by PMA, a classical NADPH oxidase stimulator, which evinces an especially high sensitivity level of neutrophils toward Ang II.…”

Section: Discussionsupporting

confidence: 93%

“…In addition, the present data demonstrate that Ang II could constitute a pivotal factor involved in the activation of neutrophils in the hypertensive state, in agreement with previous reports. 16,19,54 Another goal of this study focused on the presumptive role of ROS in the activation of kinases of the MAPK family in human neutrophils. Several lines of evidence have indicated the participation of MAPK activation in the transduction of Ang II-dependent signals in different cell types, such as vascular smooth muscle cells, 15 cardiac cells, 55 and adrenal glomerulosa cells.…”

Section: Discussionmentioning

confidence: 99%

“…9,13 Relevant ROS targets are proteins of the mitogenactivated protein kinase (MAPK) family, which are responsible for the transduction of signals from the cell membrane to the nucleus in response to classical growth factors and G-protein-coupled receptor agonists and under cellular stress conditions. 14, 15 Conflicting results have been reported about the activation of NADPH oxidase from neutrophils during the hypertensive state, and the activity of respiratory-burst oxidase has been found to become enhanced, 16 unaffected, 17 or decreased 18 compared with activity in normotensive subjects. Most studies have paid attention to the role of ROS release by vascular oxidase activity and the regulation of superoxide-induced leukocyte-endothelial cell interactions.…”

Section: Introductionmentioning

confidence: 97%

mentioning

confidence: 99%

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Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

Bekay

Álvarez

Monteseirı́n

et al. 2003

Blood

159

141

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Neutrophils are mobilized to the vascular wall during vessel inflammation. Published data are conflicting on phagocytic nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activation during the hypertensive state, and the capacity of angiotensin II (Ang II) to modulate the intracellular redox status has not been analyzed in neutrophils. We here describe that Ang II highly stimulates endogenous and extracellular O 2 ؊ production in these cells, consistent with the translocation to the cell membrane of the cytosolic components of NADPH oxidase, p47 phox , and p67 phox . The Ang II-dependent O 2 ؊ production was suppressed by specific inhibitors of AT1 receptors, of the p38MAPK and ERK1/2 pathways, and of flavin oxidases. Furthermore, Ang II induced a robust phosphorylation of p38MAPK, ERK1/2, and JNK1/2 (particularly JNK2), which was hindered by inhibitors of NADPH oxidase, tyrosine kinases, and ROS scavengers. Ang II increased cytosolic Ca 2؉ levels-released mainly from calcium stores-enhanced the syn- IntroductionAngiotensin II (Ang II), the main peptide hormone of the reninangiotensin system, induces leukocyte recruitment to the vessel wall, which constitutes a hallmark of the early stages of atherosclerosis and several hypertensive diseases. 1 In addition, it plays a regulatory role on blood pressure and circulation volume and on the proliferation of vascular smooth muscle cells. 2 Ang II acts through high-affinity cell surface receptors (AT1), which are linked to pathways classically associated with G-protein-coupled and tyrosine-kinase-mediated responses. 3 Although most studies on Ang II have been carried out in smooth muscle and endothelial cells, experimental evidence has been obtained on its effects on circulating cells. AT1 receptors for Ang II have been found recently in circulating neutrophils 4 and human peripheral monocytes, 5 and Ang II-induced cell activation in the latter has been reported. 6 In this context, the migration of leukocytes from blood to sites of inflammation and their adhesion to endothelial cells are primary events taking place during the acute inflammatory response and the pathogenesis of vascular diseases. 7 Because chronic inflammation of vessel walls is a hallmark of atherosclerosis, 8 and reactive oxygen species (ROS) such as superoxide anion (O 2 Ϫ ) and H 2 O 2 constitute the main intermediary molecules responsible for inflammation, 9 a link between atherosclerosis and ROS production has been postulated. 10 Nicotinamideadenine dinucleotide phosphate (NADPH) oxidase of phagocytes catalyzes the reduction of oxygen to O 2 Ϫ . In resting cells this enzyme is inactive, and its components are distributed between the cytosol and the membrane of secretory vesicles. When phagocytic cells are activated, the enzyme's cytosolic components associate to membrane-bound components and assemble into catalytically active NADPH oxidase. 11 It has been reported that Ang II-induced hypertrophy of vascular smooth muscle cells is mediated by both O 2 Ϫ and H 2 O 2 . 12 In addition, ROS ha...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

mentioning

confidence: 99%

See 2 more Smart Citations

Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

Bekay

Álvarez

Monteseirı́n

et al. 2003

Blood

159

141

View full text Add to dashboard Cite

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“…Our findings may explain the mechanism of the increased risk of vascular events associated with these BP characteristics, through an increase in ROS formation by MNCs. Although ROS generation has been reported to be enhanced in circulating PMNs in patients with essential hypertension (9,22,23), it is not known which patterns in diurnal BP rhythm are related to ROS formation by leukocytes (PMNs, MNCs). Using a flow cytometric method, we examined which type of oxidative stress by leukocytes was increased in the ED, DI and ND groups.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress by Peripheral Blood Mononuclear Cells Is Increased in Hypertensives with an Extreme-Dipper Pattern and/or Morning Surge in Blood Pressure

et al. 2005

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Oxygen Free Radicals and Peripheral Vascular Disease

Prasad¹

2000

Textbook of Angiology

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Enhanced activation of the respiratory burst oxidase in neutrophils from hypertensive patients

Cited by 41 publications

References 12 publications

Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

Oxidative Stress by Peripheral Blood Mononuclear Cells Is Increased in Hypertensives with an Extreme-Dipper Pattern and/or Morning Surge in Blood Pressure

Oxygen Free Radicals and Peripheral Vascular Disease

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