Plasma hydrogen peroxide production in hypertensives and normotensive subjects at genetic risk of hypertension

Lacy, Fred; O’Connor, Daniel T.; Schmid‐Schönbein, Geert W.

doi:10.1097/00004872-199816030-00006

Cited by 324 publications

(220 citation statements)

References 50 publications

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“…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 . 149,150 Plasma levels of asymmetric dimethylarginine (endothelial nitric oxide synthase inhibitor) and the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid, a marker of ROS production, were inversely correlated with microvascular endothelial dysfunction and elevated blood pressure in hypertensive patients. To further support a relationship between oxidative stress and blood pressure, Van et al 151 recently showed that myeloperoxidase is positively and independently associated with blood pressure and that this association is strongest in subjects with increased levels of oxidative markers.…”

Section: Ros and Vascular Biology In Hypertensionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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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.

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Section: Ros and Vascular Biology In Hypertensionmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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“…Previous studies have demonstrated increased vascular smooth muscle cell O 2 ·-levels with H 2 O 2 exposure . In addition, increases in systemic plasma H 2 O 2 levels have been observed in patients with cardiovascular disease (Lacy et al 1998). Oxidative stress and increased ROS are associated with multiple cardiovascular disease states.…”

Section: Cardiovascular Disease and Oxidative Stressmentioning

confidence: 99%

Mechanisms of H2O2-induced oxidative stress in endothelial cells

Coyle

Martínez

Coleman

et al. 2006

Free Radical Biology and Medicine

131

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“…Although plasma level of H 2 O 2 is usually at the nanomolar level (Lacy et al, 1998), local vascular concentration of H 2 O 2 may be much higher. According to Schraufstatter & Cochrane (1997), local concentration of superoxide (which can be rapidly converted to H 2 O 2 by superoxide dismutase) can reach 5-10 mM when polymorphonuclear leukocytes are stimulated.…”

Section: Discussionmentioning

confidence: 99%

“…Patients with uncontrolled hypertension showed a higher level of ROS (superoxide and hydrogen peroxide, H 2 O 2 ), and effective control of high blood pressure also lowered the high level of ROS to normal level (Prabha et al, 1990). Even among the normotensives, persons with a family history of hypertension exhibited a higher plasma H 2 O 2 level than those without such a family history (Lacy et al, 1998). In the spontaneously hypertensive rats (SHR), a widely used animal model of human essential hypertension, a higher level of ROS and lipid peroxidation in mesenteric arterioles and myocardium was reported (Ito et al, 1992;Suzuki et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Vascular relaxation response to hydrogen peroxide is impaired in hypertension

Gao

Zhang

Hirota

et al. 2004

British J Pharmacology

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1 In phenylephrine (1 mM)-precontracted rat superior mesenteric arteries (MA), hydrogen peroxide (H 2 O 2 , 0.3 and 1 mM) caused a biphasic response: a transient contraction followed by a relaxation. In the presence of thromboxane A 2 /prostaglandin H 2 (TP) receptor antagonist (SQ 29548), the contractile component of the biphasic response was abolished. The relaxation response to H 2 O 2 was smaller in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar-Kyoto rats (WKY). 2 The mechanisms for the attenuated relaxation to H 2 O 2 in the SHR were studied. KCl (40 mM) prevented the relaxation response. Calcium-dependent K þ channel (K Ca ) blockers (tetraethylammonium chloride, TEA; iberiotoxin, and charybdotoxin) showed a greater inhibition of H 2 O 2 relaxation in SHR than in WKY, whereas voltage-dependent K þ -channel (K v ) blocker 4-aminopyridine was more effective in inhibiting the relaxation in WKY than in SHR. 3 H 2 O 2 (1 mM) greatly enhanced the frequency and intensity of the spontaneous transient outward K þ currents in SHR MA, and the effects of H 2 O 2 were inhibited by iberiotoxin, while in WKY MA the K þ currents induced by H 2 O 2 were mainly of the K v type. The consequence of the activation of different types of K þ channel was that the net increase in mean outward K þ current density in response to H 2 O 2 was smaller in SHR than in WKY, which may account for the attenuated relaxation response to H 2 O 2 in the SHR. 4 The contractile responses of MA to TEA, iberiotoxin, and charybdotoxin were greater in SHR than in WKY. 5 In summary, an attenuated relaxation response to H 2 O 2 was found in SHR MA when compared to WKY. In contrast to the activation of K v channels in WKY, H 2 O 2 markedly enhanced K Ca activity in SHR, resulting in an attenuation of the increase in mean outward K þ current density in response to H 2 O 2 . These results suggest that alteration in K þ channel activation by reactive oxygen species may play a role in the development of hypertension in SHR.

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Plasma hydrogen peroxide production in hypertensives and normotensive subjects at genetic risk of hypertension

Abstract: Hydrogen peroxide is produced in blood plasma and elevation of its level could constitute a pathogenic factor in vascular organ damage attendant upon systemic hypertension.

Cited by 324 publications

References 50 publications

Reactive oxygen species and vascular biology: implications in human hypertension

Reactive oxygen species and vascular biology: implications in human hypertension

Mechanisms of H2O2-induced oxidative stress in endothelial cells

Vascular relaxation response to hydrogen peroxide is impaired in hypertension

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