Reactive Oxygen Species and Glucocorticoid‐induced Hypertension

Ong, Sharon L.H.; Zhang, Yi; Whitworth, Judith A.

doi:10.1111/j.1440-1681.2008.04900.x

Cited by 30 publications

(26 citation statements)

References 83 publications

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“…Under reduced BH 4 levels, eNOS synthesizes superoxide rather than NO in vitro [92] and in vivo [105,106]. There is increasing evidence for a role of oxidative stress and NO deficiency/endothelial dysfunction in experimental glucocorticoid-induced hypertension; NADPH oxidase, rather than xanthine oxidase and eNOS uncoupling, plays an important role in the pathogenesis in rats [83]. In addition, glucocorticoids decrease NO production by decreasing eNOS gene transcription [28].…”

Section: Glucocorticoidsmentioning

confidence: 98%

How mental stress affects endothelial function

Toda¹,

Nakanishi-Toda

2011

Pflugers Arch - Eur J Physiol

109

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Mental stress is an important factor contributing to recognized mechanisms underlying cardiovascular events. Among these, stress-related endothelial dysfunction is an early risk factor that predicts future development of severe cardiovascular disorders. Acute mental stress by a variety of tests impairs endothelial function in humans, although the opposite results have been reported by some investigators. Chronic stress always deteriorates endothelial function in humans and experimental animals. Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation. Catecholamines do not directly affect endothelial function but impair its function when blood pressure elevation by the amines is sustained. Endogenous opioids favorably affect endothelial function, which counteract deteriorating effects of other stress hormones and mediators. Inhibition of cortisol and endothelin-1 production, prevention of pro-inflammatory mediator accumulation, hypnotics, mirthful laughter, humor orientation, and lifestyle modification would contribute to the prevention and treatment for stress-related endothelial dysfunction and future serious cardiovascular disease.

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Section: Glucocorticoidsmentioning

confidence: 98%

How mental stress affects endothelial function

Toda¹,

Nakanishi-Toda

2011

Pflugers Arch - Eur J Physiol

109

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“…Hypertension increases endothelial oxidative stress and inflammation and leads to worse stroke outcomes and higher mortality [210][211][212][213][214][215][216][217][218][219][220]. Studies investigating the underlying pathophysiology of hypertension indicates the involvement of neuroimmune interactions.…”

Section: Hypertensionmentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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Historically, the brain has been considered an immune-privileged organ separated from the peripheral immune system by the blood-brain barrier. However, immune responses do occur in the brain in neurological conditions in which the integrity of the blood-brain barrier is compromised, exposing the brain to peripheral antigens and endogenous danger signals. While most of the associated pathological processes occur in the central nervous system, it is now clear that peripheral immune cells, especially mononuclear phagocytes, that infiltrate into the injury site play a key role in modulating the progression of primary brain injury development. As inflammation is a necessary and critical component for the subsequent injury resolution process, understanding the contribution of mononuclear phagocytes on the regulation of inflammatory responses may provide novel approaches for potential therapies. Furthermore, predisposed comorbid conditions at the time of stroke cause the alteration of stroke-induced immune and inflammatory responses and subsequently influence stroke outcome. In this review, we summarize a role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions.

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“…Furthermore, these effects are abolished by adrenalectomy or treatment with the GR antagonist RU486 (Suzuki et al 1995). Oxidative stress and nitric oxide deficiency are emerging as key components in the pathogenesis of glucocorticoid-induced hypertension (Ong et al 2008). Nitric oxide deficiency in models of glucocorticoidinduced hypertension is thought to be due to decreased L-arginine availability and reduced endothelial nitric oxide synthase and inducible nitric oxide synthase gene expression (Whitworth et al 2002).…”

Section: Glucocorticoid-induced Hypertension and Macrophagesmentioning

confidence: 99%

Corticosteroid receptors, macrophages and cardiovascular disease

Rickard¹,

Young²

2009

Journal of Molecular Endocrinology

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The mineralocorticoid receptor (MR) and glucocorticoid receptor are ligand-activated transcription factors that have important physiological and pathophysiological actions in a broad range of cell types including monocytes and macrophages. While the glucocorticoids cortisol and corticosterone have well-described anti-inflammatory actions on both recruited and tissue resident macrophages, a role for the mineralocorticoid aldosterone in these cells is largely undefined. Emerging evidence, however, suggests that MR signalling may promote pro-inflammatory effects. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on diseases involving inflammation, with a particular focus on cardiovascular disease.

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Reactive Oxygen Species and Glucocorticoid‐induced Hypertension

Cited by 30 publications

References 83 publications

How mental stress affects endothelial function

How mental stress affects endothelial function

Microglia and Monocyte-Derived Macrophages in Stroke

Corticosteroid receptors, macrophages and cardiovascular disease

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