Mechanism of vascular dysfunction due to circulating factors in women with pre-eclampsia

2016 ◽  
Vol 130 (7) ◽  
pp. 539-549 ◽  
Author(s):  
Cindy K. Kao ◽  
Jude S. Morton ◽  
Anita L. Quon ◽  
Laura M. Reyes ◽  
Patricio Lopez-Jaramillo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Prostaglandin H Synthase ◽  
Prostaglandin H ◽  
Nitric Oxide Bioavailability

Circulating factors in the plasma of pre-eclamptic women contribute to vascular dysfunction by increasing oxidative stress, which is associated with a reduction in nitric oxide bioavailability and an increase in prostaglandin H synthase-dependent vasoconstrictors.

scholarly journals Doxycycline ameliorates 2K-1C hypertension-induced vascular dysfunction in rats by attenuating oxidative stress and improving nitric oxide bioavailability

Nitric Oxide ◽  
2012 ◽  
Vol 26 (3) ◽  
pp. 162-168 ◽  
Author(s):  
Michele M. Castro ◽  
Elen Rizzi ◽  
Carla S. Ceron ◽  
Danielle A. Guimaraes ◽  
Gerson J. Rodrigues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Nitric Oxide Bioavailability

scholarly journals Development of an Adverse Outcome Pathway for the Onset of Hypertension by Oxidative Stress-Mediated Perturbation of Endothelial Nitric Oxide Bioavailability

2017 ◽  
Vol 3 (1) ◽  
pp. 131-148 ◽  
Author(s):  
Frazer J. Lowe ◽  
Karsta Luettich ◽  
Marja Talikka ◽  
Vy Hoang ◽  
Linsey E. Haswell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Adverse Outcome ◽  
Adverse Outcome Pathway ◽  
Endothelial Nitric Oxide ◽  
Nitric Oxide Bioavailability

scholarly journals Regional Distribution of Prostaglandin H Synthase-2 and Neuronal Nitric Oxide Synthase in Piglet Brain

1998 ◽  
Vol 43 (5) ◽  
pp. 683-689 ◽  
Author(s):  
Rózsa Dégì ◽  
Ferenc Bari ◽  
Tracy C Beasley ◽  
Nishadi Thrikawala ◽  
Clara Thore ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Regional Distribution ◽  
Neuronal Nitric Oxide Synthase ◽  
Prostaglandin H Synthase ◽  
Prostaglandin H ◽  
Oxide Synthase

Nitric Oxide Produced by Endothelial Cells Increases Production of Eicosanoids Through Activation of Prostaglandin H Synthase

1995 ◽  
Vol 77 (2) ◽  
pp. 274-283 ◽  
Author(s):  
Sandra T. Davidge ◽  
Philip N. Baker ◽  
Margaret K. McLaughlin ◽  
James M. Roberts
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Prostaglandin H Synthase ◽  
Prostaglandin H

scholarly journals Depletion of iNOS-derived nitric oxide by prostaglandin H synthase-2 in inflammation-activated J774.2 macrophages through lipohydroperoxidase turnover

2005 ◽  
Vol 385 (3) ◽  
pp. 815-821 ◽  
Author(s):  
Stephen R. CLARK ◽  
Peter B. ANNING ◽  
Marcus J. COFFEY ◽  
Andrew G. ROBERTS ◽  
Lawrence J. MARNETT ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Mammalian Cells ◽  
Biological Effects ◽  
Interferon Γ ◽  
Dependent Manner ◽  
Prostaglandin H Synthase ◽  
Prostaglandin H ◽  
20 Nm ◽  
Pro Inflammatory Cytokines

PGHS-2 (prostaglandin H synthase-2) is induced in mammalian cells by pro-inflammatory cytokines in tandem with iNOS [high-output (‘inducible’) nitric oxide synthase], and is co-localized with iNOS and nitrotyrosine in human atheroma macrophages. Herein, murine J774.2 macrophages incubated with lipopolysaccharide and interferon γ showed induction of PGHS-2 and generated NO using iNOS that could be completely depleted by 12(S)-HPETE [12(S)-hydroperoxyeicosatetraenoic acid; 2.4 μM] or hydrogen peroxide (500 μM) (0.42±0.084 and 0.38±0.02 nmol·min−1·106 cells−1 for HPETE and H2O2 respectively). COS-7 cells transiently transfected with human PGHS-2 also showed HPETE- or H2O2-dependent NO decay (0.44±0.016 and 0.20±0.04 nmol·min−1·106 cells−1 for 2.4 μM HPETE and 500 μM H2O2 respectively). Finally, purified PGHS-2 consumed NO in the presence of HPETE or H2O2 (168 and 140 μM·min−1·μM enzyme−1 for HPETE and H2O2 respectively), in a haem-dependent manner, with 20 nM enzyme consuming up to 4 μM NO. Km (app) values for NO and 15(S)-HPETE were 1.7±0.2 and 0.45±0.16 μM respectively. These data indicate that PGHS-2 catalytically consumes NO during peroxidase turnover and that pro-inflammatory cytokines simultaneously upregulate NO synthesis and degradation pathways in murine macrophages. Catalytic NO consumption by PGHS-2 represents a novel interaction between NO and PGHS-2 that may impact on the biological effects of NO in vascular signalling and inflammation.

scholarly journals Cinnamaldehyde Ameliorates Vascular Dysfunction in Diabetic Mice by Activating Nrf2

2020 ◽  
Vol 33 (7) ◽  
pp. 610-619 ◽  
Author(s):  
Peijian Wang ◽  
Yi Yang ◽  
Dan Wang ◽  
Qiyuan Yang ◽  
Jindong Wan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Mesenteric Arteries ◽  
Heme Oxygenase 1 ◽  
No Production ◽  
Related Factor ◽  
Diabetic Mice ◽  
Quinone Oxidoreductase ◽  
Nrf2 Signaling Pathway

Abstract BACKGROUND Oxidative stress is known to be associated with the development of diabetes. Cinnamaldehyde (CA) is a spice compound in cinnamon that enhances the antioxidant defense against reactive oxygen species (ROS) by activating nuclear factor erythroid-related factor 2 (Nrf2), which has been shown to have a cardioprotection effect. However, the relationship between CA and Nrf2 in diabetic vascular complications remains unclear. METHODS Leptin receptor-deficient (db/db) mice were fed normal chow or diet containing 0.02% CA for 12 weeks. The vascular tone, blood pressure, superoxide level, nitric oxide (NO) production, renal morphology, and function were measured in each group. RESULTS CA remarkably inhibited ROS generation, preserved NO production, increased phosphorylated endothelial nitric oxide synthase (p-eNOS), attenuated the upregulation of nitrotyrosine, P22 and P47 in aortas of db/db mice, and apparently ameliorated the elevation of type IV collagen, TGF-β1, P22, and P47 in kidney of db/db mice. Feeding with CA improved endothelium-dependent relaxation of aortas and mesenteric arteries, and alleviated the remodeling of mesenteric arteries in db/db mice. Additionally, dietary CA ameliorated glomerular fibrosis and renal dysfunction in diabetic mice. Nrf2 and its targeted genes heme oxygenase-1 (HO-1) and quinone oxidoreductase-1 (NQO-1) were slightly increased in db/db mice and further upregulated by CA. However, these protective effects of CA were reversed in Nrf2 downregulation mice. CONCLUSIONS A prolonged diet of CA protects against diabetic vascular dysfunction by inhibiting oxidative stress through activating of Nrf2 signaling pathway in db/db mice.

Gender differences in myogenic tone in superoxide dismutase knockout mouse: animal model of oxidative stress

2004 ◽  
Vol 287 (1) ◽  
pp. H40-H45 ◽  
Author(s):  
Sukrutha Veerareddy ◽  
Christy-Lynn M. Cooke ◽  
Philip N. Baker ◽  
Sandra T. Davidge
Keyword(s):  
Oxidative Stress ◽  
Vascular Function ◽  
Vascular Tone ◽  
Vascular Dysfunction ◽  
Mesenteric Arteries ◽  
Myogenic Tone ◽  
Intracellular Enzyme ◽  
Male And Female ◽  
Prostaglandin H ◽  
Myogenic Regulation

Oxidative stress mediated by prooxidants has been implicated in the pathogenesis of vascular disorders. However, the effect of prooxidants on myogenic regulation of vascular function and the differential influence of gender is not known. SOD, an intracellular enzyme, restricts excess prooxidant levels and may limit vascular dysfunction. We therefore tested the effects of Cu,Zn SOD deficiency on vascular tone in both male and female SOD knockout (SOD−/−) mice. We hypothesized that myogenic tone would be enhanced in SOD−/− mice by excess prooxidants compared with wild-type control mice. Indeed, resistance-sized mesenteric arteries from SOD−/− mice exhibited enhanced myogenic tone compared with control mice. Myogenic tone was lower in female than male control mice. Interestingly, this gender effect was absent in SOD−/− mice, such that myogenic tone of mesenteric arteries from females was equated to that of arteries from males. Furthermore, the pathways that modulate myogenic tone were diverse. In both male and female control mice, inhibition of prostaglandin H synthase (PGHS) and nitric oxide synthase (NOS) pathways enhanced myogenic tone. In female SOD−/− mice, inhibition of PGHS and NOS pathways enhanced myogenic tone to a greater extent compared with control mice. Conversely, in male SOD−/− mice, NOS and PGHS inhibition did not alter tone and only inhibition of gap junctions enhanced myogenic tone. In conclusion, this study revealed enhanced myogenic tone in SOD−/− mice compared with control mice. Furthermore, Cu,Zn SOD deficiency particularly enhanced myogenic tone in female mice such that their vascular tone attained the level of male SOD−/− mice, possibly mediated by prooxidants.

Estrogen replacement reduces PGHS-2-dependent vasoconstriction in the aged rat

2002 ◽  
Vol 283 (3) ◽  
pp. H893-H898 ◽  
Author(s):  
Stephen J. Armstrong ◽  
Yunlong Zhang ◽  
Ken G. Stewart ◽  
Sandra T. Davidge
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Mesenteric Arteries ◽  
Estrogen Replacement ◽  
Aged Rat ◽  
Arterial Relaxation ◽  
Prostaglandin H ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Endothelium Dependent Relaxation

The reduction in estrogen in postmenopausal women contributes to an increase in vascular dysfunction. Models of aging have shown that this is due, in part, to increased prostaglandin H synthase (PGHS)-dependent vasoconstriction. We showed previously that inducible PGHS-2-dependent vasoconstriction is increased with aging. In the present study, we hypothesized that estrogen suppresses PGHS-2-dependent constriction in the aged rat. Isolated mesenteric arteries from placebo- or estrogen-treated, ovariectomized aged (24 mo) Fisher rats were assessed for endothelium-dependent relaxation in the absence or presence of PGHS inhibitors. PGHS inhibition (meclofenamate, 1 μmol/l) enhanced methacholine-induced relaxation only in the placebo group. Specific PGHS-2 inhibition (NS-398, 10 μmol/l) increased arterial relaxation to a greater extent than PGHS-1 inhibition (valeryl salicylate, 3 mmol/l). Estrogen prevented the PGHS-dependent constrictor effect but did not enhance nitric oxide-dependent relaxation in this model. PGHS-1 and endothelial nitric oxide synthase were not altered by estrogen, whereas PGHS-2 expression was decreased in the estrogen-replaced rats ( P < 0.05). In summary, estrogen replacement improved vasodilation in aged rats by decreasing PGHS-dependent constriction.

Nitric oxide enhances prostaglandin-H synthase-1 activity by a heme-independent mechanism: Evidence implicating nitrosothiols

1995 ◽  
Vol 117 (12) ◽  
pp. 3340-3346 ◽  
Author(s):  
David P. Hajjar ◽  
Harry M. Lander ◽  
S. Freida A. Pearce ◽  
Rita Upmacis ◽  
Kenneth B. Pomerantz
Keyword(s):  
Nitric Oxide ◽  
Prostaglandin H Synthase ◽  
Independent Mechanism ◽  
Prostaglandin H
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