Vascular Actions of Nitric Oxide as Affected by Exposure to Alcohol

Toda, Noboru; Ayajiki, Kazuhide

doi:10.1093/alcalc/agq028

Cited by 77 publications

(55 citation statements)

References 89 publications

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“…Chronic stress could lead to an unhealthy lifestyle: smoking, excessive alcohol drinking, overeating, and insomnia, all factors that further impair endothelial function and increase cardiovascular risk [117,121]. Lifestyle modifications that included consumption of low-fat, high antioxidant, and high fiber diets; doing moderate aerobic exercise; and stress management for 6 months ameliorated oxidative stress and serum lipids in patients with coronary artery disease; in addition, endothelial cell survival was increased, while intracellular ROS production was decreased in vitro as determined by examining the serum of the lifestyle-modified patients [111].…”

Section: Lifestylementioning

confidence: 99%

How mental stress affects endothelial function

Toda¹,

Nakanishi-Toda

2011

Pflugers Arch - Eur J Physiol

106

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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: Lifestylementioning

confidence: 99%

How mental stress affects endothelial function

Toda¹,

Nakanishi-Toda

2011

Pflugers Arch - Eur J Physiol

106

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“…A recent study showed that impairment of NO action promotes the genesis of cardiovascular diseases [31]. The synthesis of NO is blocked by inhibition of the NOS active site with guanidino-substituted analogues of L-arginine, such as asymmetric dimethylarginine (ADMA) [29].…”

Section: Protease Systemmentioning

confidence: 99%

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

et al. 2011

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“…The adverse effects would be related to the high consumption of the so-called heavy drinks (alcohol consumption ³100 g/dL). Toda and Ayajiki (2010), in a review study, when evaluating the association of NO vascular action and alcohol consumption, observed that NO concentration was inverse to alcohol consumption. That is, low alcohol concentrations determined increased endothelial NO rates by increased activation and NOS expression.…”

Section: Discussionmentioning

confidence: 99%

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

Campedelli¹,

Silva²,

Rodrigues³

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Atherosclerotic and its cardiovascular complications are responsible for 17.5 million deaths a year, according to the World Health Organization. There is consensus that atherosclerosis involves multiple pathogenic processes initiated by endothelial dysfunction, with inflammation and vascular proliferation determining alterations in the matrix, with consequent formation of the atheromatous plaque and its clinical implications. Risk factors such as hypertension, diabetes mellitus, dyslipidemia, and smoking are widely known. Currently, genotyping, which is not directly related to these factors, is not accepted to estimate the risk of cardiovascular diseases, but strong evidence indicates several polymorphic genes as factors of risk and progression leading to complications of the disease. Among the genes involved, eNOS (endothelial nitric oxide synthase gene), which is responsible for the production of endothelial nitric oxide (an important arterial vasodilator), when presented in polymorphic variation can determine production, malfunction, and predisposition to atherosclerosis. In the present study, we analyzed the G894T polymorphism of the eNOS gene in groups of individuals diagnosed with atherosclerosis and in a control group. We collected 200 blood samples from patients previously diagnosed with atherosclerosis and 100 samples formed the control group. The genotyping analysis for polymorphism of the eNOS gene was determined by PCR. We considered variables such as gender, smoking, smoking history, and alcohol consumption; statistical differences were found in the distribution of case and control groups (P = 0.0378) and in non-smoking patients (P = 0.0263). In the other associations, no statistically significant difference was found. In the population studied, the frequency of the heterozygous genotype (GT) was much higher than in the other populations (GG and TT) in both groups (case and control). The GG genotype showed greater susceptibility to atherosclerosis. Association of the GG genotype in non-smokers also showed greater susceptibility. Gender, alcohol consumption, smoking, and smoking history did not influence atherosclerosis.

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Vascular Actions of Nitric Oxide as Affected by Exposure to Alcohol

Cited by 77 publications

References 89 publications

How mental stress affects endothelial function

How mental stress affects endothelial function

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

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