Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats

Xu, Tao; Lan, Xiao-hong; Guan, Yongjun; Zhang, Sai-long; Wang, Xia

doi:10.1038/aps.2015.5

Cited by 12 publications

(10 citation statements)

References 40 publications

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“…The health care risk associated cigarette smoke for CVD is exaggerated by obesity or type II diabetic mellitus[ 6 , 19 , 20 ]. Nicotine has been suggested to participate in many of the adverse effects of smoke on the CV system[ 7 ], although there are also opposite reports that chronic nicotine treatment may have some beneficial vascular effects[ 35 ] We and others[ 3 , 36 ] have shown that chronic nicotine treatment promotes atherosclerotic lesion formation in apo E -/- mice. Nicotine replacement therapy (NRT) is widely used for smoking cessation[ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα

Liu

Zhou

et al. 2017

PLoS ONE

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Obesity and cigarette smoke are major cardiovascular (CV) risk factors and, when coexisting in the same individuals, have additive/synergistic effects upon CVD. We studied the mechanisms involved in nicotine enhancement of CVD in Sprague Dawley rats with diet–induced obesity. The rats were fed either a high fat (HFD) or normal rat chow diet with or without nicotine (100 mg/L in drinking water) for 20 weeks. HFD rats developed central obesity, increased systolic blood pressure (SBP), aortic superoxide (O2-) production, and impaired endothelial nitric oxide synthase (eNOS) and endothelium-dependent relaxation to acetylcholine (EDR). Nicotine further increased SBP, O2- and impaired eNOS and EDR in obese rats. In the peritoneal macrophages from obese rats, tumor necrosis factor (TNF) α, interleukin 1β and CD36 were increased, and were further increased in nicotine-treated obese rats. Using PCR array we found that 3 of 84 target proinflammatory genes were increased by 2–4 fold in the aorta of obese rats, 11 of the target genes were further increased in nicotine-treated obese rats. HUVECs, incubated with conditioned medium from the peritoneal macrophages of nicotine treated-obese rats, exhibited reduced eNOS and increased NADPH oxidase subunits gp91phox and p22phox expression. Those effects were partially prevented by adding anti-TNFα antibody to the conditioned medium. Our results suggest that nicotine aggravates the CV effects of diet–induced obesity including the oxidative stress, vascular inflammation and endothelial dysfunction. The underlying mechanisms may involve in targeting endothelium by enhancement of macrophage-derived TNFα.

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Section: Discussionmentioning

confidence: 99%

Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα

Liu

Zhou

et al. 2017

PLoS ONE

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“…the GC/PKG pathway. Two animal models have demonstrated endothelial dysfunction in nicotine exposed rats [187,188]. These studies found an attenuated effect of NO-mediated vasodilation through upregulated Ca 2+ channels in vascular smooth muscle cells and an altered PKG-pathway.…”

Section: Forearm Blood Flowmentioning

confidence: 98%

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

et al. 2016

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“…In addition to being the largest reservoir for energy storage, adipose tissue is a highly active endocrine organ that synthesizes and secretes proteins/peptides termed adipokines 10 , 59 . Adipokines participate in the regulation of multiple physiological functions, including metabolism, insulin sensitivity, cardiocerebrovascular function, immunity and inﬂammation 10 , 60 . Dysregulated production or secretion of adipokines is associated with the pathogenesis of obesity-linked disorders 61 , 62 .…”

Section: Function Of Metrnlmentioning

confidence: 99%

Metrnl: a secreted protein with new emerging functions

et al. 2016

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Secreted proteins play critical roles in physiological and pathological processes and can be used as biomarkers and therapies for aging and disease. Metrnl is a novel secreted protein homologous to the neurotrophin Metrn. But this protein, unlike Metrn that is mainly expressed in the brain, shows a relatively wider distribution in the body with high levels of expression in white adipose tissue and barrier tissues. This protein plays important roles in neural development, white adipose browning and insulin sensitization. Based on its expression and distinct functions, this protein is also called Cometin, Subfatin and Interleukin 39, which refer to its neurotrophic effect, adipokine function and the possible action as a cytokine, respectively. The spectrum of Metrnl functions remains to be determined, and the mechanisms of Metrnl action need to be elucidated. In this review, we focus on the discovery, structural characteristics, expression pattern and physiological functions of Metrnl, which will assist in developing this protein as a new therapeutic target or agent.

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Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats

Abstract: Chronic nicotine treatment enhances vascular smooth muscle relaxation of rats via activation of PKG pathway.

Cited by 12 publications

References 40 publications

Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα

Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

Metrnl: a secreted protein with new emerging functions

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