Oxidative Stress in Leukocytes Is a Possible Link Between Blood Pressure, Blood Glucose, and C-Reacting Protein

Yasunari, Kenichi; Maeda, Kensaku; Nakamura, Munehiro; Yoshikawa, Junichi

doi:10.1161/hy0302.104670

Cited by 188 publications

(131 citation statements)

References 24 publications

Supporting

Mentioning

123

Contrasting

Order By: Relevance

“…Both ED and surge-type morning BP hypertensives are known to be at increased risk for vascular events (1, 2). PMNs have not been clearly identified as contributing to brain damage (14,15), but MNCs have been found in damaged brain tissues (19), which is consistent with our previous findings that ROS formation by PMNs and MNCs are differently regulated; ROS formation by PMNs is related with BP (20) and hemoglobin A1C, but not with blood glucose or CRP (9). ROS formation by MNCs is related to CRP (9).…”

Section: Discussionsupporting

confidence: 81%

See 1 more Smart Citation

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

Self Cite

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 81%

“…Hypertension is known to increase oxidative stress in polymorphonuclear leukocytes (PMNs) and mononuclear cells (MNCs) (9,10). PMNs are one of the main types of inflammatory cells.…”

Section: Introductionmentioning

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

Self Cite

View full text Add to dashboard Cite

“…[144][145][146] Polymorphonuclear leukocyte-and platelet-derived O 2 À , which also participate in vascular oxidative stress and inflammation, are increased in hypertensive patients. 147 Hypertensive patients exhibit a significantly higher production of plasma H 2 O 2 than normotensive subjects. 148 Additionally, normotensive subjects with a family history of hypertension have greater H 2 O 2 production than blood pressure-matched normotensives without a family history of hypertension, suggesting that there may be a genetic component that leads to elevated production of H 2 O 2 .…”

Section: Ros and Vascular Biology In Hypertensionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

View full text Add to dashboard Cite

Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

show abstract

“…3 Assessment of antioxidant activities and lipid peroxidation byproducts in hypertensives indicates an excessive amount of ROS and a reduction of antioxidant mechanism activity in blood, as well as in several other cellular systems, 4 including not only vascular wall cells, 5 but also those cells found in circulating blood. 6,7 Increased OX of hypertensive subjects improved with the antihypertensive treatment, and extending treatment over time increased the beneficial impact of treatment. 8 The clinical relevance of OX and of antioxidant mechanisms has most recently received support in a paper that linked the activity of glutathione peroxidase type 1 (GPx1), one of the most important cytoplasmic antioxidant enzymatic systems, to the risk of CV events in a population with coronary heart disease.…”

Section: Introductionmentioning

confidence: 99%

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

et al. 2006

View full text Add to dashboard Cite

The objective of the present study was to analyze the impact of metabolic syndrome (MS) and its individual components on oxidative stress (OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehide, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysad erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.

show abstract

Oxidative Stress in Leukocytes Is a Possible Link Between Blood Pressure, Blood Glucose, and C-Reacting Protein

Cited by 188 publications

References 24 publications

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

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

Reactive oxygen species and vascular biology: implications in human hypertension

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

Contact Info

Product

Resources

About