Aging-related endothelial dysfunction in the aorta from female senescence-accelerated mice is associated with decreased nitric oxide synthase expression

Novella, Susana; Dantas, Ana Paula; Segarra, Gloria; Vidal‐Gómez, Xavier; Mompeón, Ana; Garabito, Manel; Hermenegildo, Carlos; Medina, Pascual

doi:10.1016/j.exger.2013.08.003

Cited by 48 publications

(37 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The isoform eNOS is constitutively expressed in the vasculature and increased contractility in response to phenylephrine is described when eNOS is down-regulated (Novella et al, 2013). This seems not to be the case in our study since Results are mean ± SEM of n ¼ 7 for control and n ¼ 11 for stressed rats.…”

Section: Phenylephrinecontrasting

confidence: 52%

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress

Carda

Marchi

Rizzi

et al. 2015

Stress

View full text Add to dashboard Cite

We hypothesized that acute stress would induce endothelial dysfunction. Male Wistar rats were restrained for 2 h within wire mesh. Functional and biochemical analyses were conducted 24 h after the 2-h period of restraint. Stressed rats showed decreased exploration on the open arms of an elevated-plus maze (EPM) and increased plasma corticosterone concentration. Acute restraint stress did not alter systolic blood pressure, whereas it increased the in vitro contractile response to phenylephrine and serotonin in endothelium-intact rat aortas. NG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase, NOS, inhibitor) did not alter the contraction induced by phenylephrine in aortic rings from stressed rats. Tiron, indomethacin and SQ29548 reversed the increase in the contractile response to phenylephrine induced by restraint stress. Increased systemic and vascular oxidative stress was evident in stressed rats. Restraint stress decreased plasma and vascular nitrate/nitrite (NOx) concentration and increased aortic expression of inducible (i) NOS, but not endothelial (e) NOS. Reduced expression of cyclooxygenase (COX)-1, but not COX-2, was observed in aortas from stressed rats. Restraint stress increased thromboxane (TX)B(2) (stable TXA(2) metabolite) concentration but did not affect prostaglandin (PG)F2α concentration in the aorta. Restraint reduced superoxide dismutase (SOD) activity, whereas concentrations of hydrogen peroxide (H(2)O(2)) and reduced glutathione (GSH) were not affected. The major new finding of our study is that restraint stress increases vascular contraction by an endothelium-dependent mechanism that involves increased oxidative stress and the generation of COX-derived vasoconstrictor prostanoids. Such stress-induced endothelial dysfunction could predispose to the development of cardiovascular diseases.

show abstract

Section: Phenylephrinecontrasting

confidence: 52%

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress

Carda

Marchi

Rizzi

et al. 2015

Stress

View full text Add to dashboard Cite

show abstract

“…For example, increased contractility in response to phenylephrine is described when eNOS is down-regulated in the vasculature [34,35]. Similarly, decreased vascular expression of nNOS is associated with a hyper-reactivity to phenylephrine [36].…”

Section: Discussionmentioning

confidence: 96%

Contribution of oxidative stress and prostanoids in endothelial dysfunction induced by chronic fluoxetine treatment

Simplicio

Resstel²,

Tirapelli³

et al. 2015

Vascular Pharmacology

View full text Add to dashboard Cite

“…Similarly to oxidative damage, nitrosative damage – that caused by reactive nitrogen species (RNS), such as nitric oxide – has been suggested to also contribute to age-related diseases, namely, hepatic steatosis and apoptosis (Abdelmegeed et al, 2016), as well as functional and structural changes in the cardiovascular system (Novella et al, 2013; Surikow et al, 2015). Additionally, it has also been associated to impairments in sleep homeostasis (Rytkönen et al, 2010), psychological disorders (Maurya et al, 2016) and dementia (Mangialasche et al, 2009).…”

Section: Theories Of Aging and How They Shape The Definitions Of Smentioning

confidence: 99%

A synopsis on aging—Theories, mechanisms and future prospects

Costa

Vitorino

Silva³

et al. 2016

Ageing Research Reviews

327

170

View full text Add to dashboard Cite

Answering the question as to why we age is tantamount to answering the question of what is life itself. There are countless theories as to why and how we age, but, until recently, the very definition of aging – senescence – was still uncertain. Here, we summarize the main views of the different models of senescence, with a special emphasis on the biochemical processes that accompany aging. Though inherently complex, aging is characterized by numerous changes that take place at different levels of the biological hierarchy. We therefore explore some of the most relevant changes that take place during aging and, finally, we overview the current status of emergent aging therapies and what the future holds for this field of research. From this multi-dimensional approach, it becomes clear that an integrative approach that couples aging research with systems biology, capable of providing novel insights into how and why we age, is necessary.

show abstract

Aging-related endothelial dysfunction in the aorta from female senescence-accelerated mice is associated with decreased nitric oxide synthase expression

Cited by 48 publications

References 31 publications

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress

Contribution of oxidative stress and prostanoids in endothelial dysfunction induced by chronic fluoxetine treatment

A synopsis on aging—Theories, mechanisms and future prospects

Contact Info

Product

Resources

About