Sex differences in the role of NADPH oxidases in endothelium-dependent vasorelaxation in porcine isolated coronary arteries

Wong, Pui San; Randall, Michael D.; Roberts, Richard E.

doi:10.1016/j.vph.2015.04.001

Cited by 30 publications

(24 citation statements)

References 39 publications

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“…Hemorrhage volume was not calculated by adding the areas of bleeding in all coronal brain slices in our study. In addition, NOX-generated ROS play a role in the development of age-related vascular diseases and are involved in the regulation of endothelial function with sex differences attributed to the differential expression of NOX isoforms 27 28. Whether the protective effects of NOX inhibition last beyond 24 h in young and aging rats of both sexes requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

NADPH oxidase inhibitor improves outcome of mechanical reperfusion by suppressing hemorrhagic transformation

Tuo

Zhong

Chen

et al. 2016

J NeuroIntervent Surg

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Section: Discussionmentioning

confidence: 99%

NADPH oxidase inhibitor improves outcome of mechanical reperfusion by suppressing hemorrhagic transformation

Tuo

Zhong

Chen

et al. 2016

J NeuroIntervent Surg

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“…For example, a recent study on the effects of chronic restraint stress on vascular function showed that ML171 (0.5 μM) reduced AngII-initiated vasoconstriction in rat carotid arteries in the presence and absence of endothelium, implying that Nox1-derived ROS positively influence AngII-mediated contraction in carotid arterial smooth muscle cells [237]. Another study comparing endothelial function of coronary arteries from male and female pigs reported that 100 μM ML171 enhanced bradykinin-induced endothelium-dependent relaxation in male rather than female porcine coronary arteries [238]. Nevertheless, it is not clear whether Nox1 alone played a role in suppressing vasodilation, since 100 μM of ML171 is high enough to abolish the activity of other Nox isozymes as well as xanthine oxidase [236].…”

Section: Nox Inhibitors As Therapeutics For Microvascular Diseasesmentioning

confidence: 99%

Microvascular NADPH oxidase in health and disease

Pagano

2017

Free Radical Biology and Medicine

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The systemic and cerebral microcirculation contribute critically to regulation of local and global blood flow and perfusion pressure. Microvascular dysfunction, commonly seen in numerous cardiovascular pathologies, is associated with alterations in the oxidative environment including potentiated production of reactive oxygen species (ROS) and subsequent activation of redox signaling pathways. NADPH oxidases (Noxs) are a primary source of ROS in the vascular system and play a central role in cardiovascular health and disease. In this review, we focus on the roles of Noxs in ROS generation in resistance arterioles and capillaries, and summarize their contributions to microvascular physiology and pathophysiology in both systemic and cerebral microcirculation. In light of the accumulating evidence that Noxs are pivotal players in vascular dysfunction of resistance arterioles, selectively targeting Nox isozymes could emerge as a novel and effective therapeutic strategy for preventing and treating microvascular diseases.

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“…; Wong et al. ). In this regard, although a small sample number and mismatched age are not suitable for making a conclusion, similar influences of t‐BuOOH on vascular reactivity to BAY compound were observed in coronary arteries obtained from male (Fig.…”

Section: Discussionmentioning

confidence: 98%

“…This may be because male coronary arteries, compared to female coronary arteries, are intrinsically under high oxidative stress conditions (Wong et al. ). Age mismatch may not be a cause of the sex difference in t‐BuOOH‐induced effects because our recent study showed that aging does not affect vascular sGC redox equilibrium (Shimosato et al.…”

Section: Discussionmentioning

confidence: 99%

Soluble guanylate cyclase redox state under oxidative stress conditions in isolated monkey coronary arteries

Tawa

Okamura

2016

Pharmacology Res & Perspec

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Coronary artery disease is associated with oxidative stress due to the excessive generation of free radicals in the vascular wall. This study investigated the impact of tert‐butyl hydroperoxide (t‐BuOOH), a peroxyl radical generator, on the redox state of soluble guanylate cyclase (sGC) in isolated monkey coronary arteries. Helically cut strips of endothelium‐intact monkey coronary arteries treated with the nitric oxide synthase inhibitor NG‐nitro‐L‐arginine (10 μmol/L) were exposed for approximately 60 min to either no drug or t‐BuOOH (100 μmol/L) in the presence and absence of α‐tocopherol (300 μmol/L). Relaxation and cGMP levels in response to the sGC stimulator BAY 41‐2272 and the sGC activator BAY 60‐2770 were assessed by organ chamber technique and enzyme immunoassay, respectively. The relaxant response to BAY 41‐2272 was significantly impaired by the exposure to t‐BuOOH, whereas the response to BAY 60‐2770 was significantly augmented. In addition, vascular cGMP accumulation caused by BAY 41‐2272 was decreased by the exposure to t‐BuOOH, whereas for BAY 60‐2770, it was increased. These effects of t‐BuOOH were abolished by coincubation with α‐tocopherol. Furthermore, correlations were observed between BAY compound‐induced relaxant magnitudes and cGMP levels. Therefore, it is concluded that increased oxidative stress leads to disruption of the sGC redox state in monkey coronary arteries. This finding is of great importance for understanding coronary physiology in primates.

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Sex differences in the role of NADPH oxidases in endothelium-dependent vasorelaxation in porcine isolated coronary arteries

Cited by 30 publications

References 39 publications

NADPH oxidase inhibitor improves outcome of mechanical reperfusion by suppressing hemorrhagic transformation

NADPH oxidase inhibitor improves outcome of mechanical reperfusion by suppressing hemorrhagic transformation

Microvascular NADPH oxidase in health and disease

Soluble guanylate cyclase redox state under oxidative stress conditions in isolated monkey coronary arteries

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