ArticleJournal of applied physiology (Bethesda, Md. : 1985)2010
Exercise training restores impaired dilator responses of cerebral arterioles during chronic exposure to nicotine.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- The Physiological and Molecular Links Between Physical Activity and Brain Health: A Review.Neuroscience insights · 2023Review
- Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021Review
- Dynamics of middle cerebral artery blood flow velocity during moderate-intensity exercise.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Magnetic resonance imaging biomarkers of exercise-induced improvement of oxidative stress and inflammation in the brain of old high-fat-fed ApoEThe Journal of physiology · 2016Article
- NADPH Oxidase Activity in Cerebral Arterioles Is a Key Mediator of Cerebral Small Vessel Disease-Implications for Prevention.Healthcare (Basel, Switzerland) · 2015Review
- Do we age because we have mitochondria?Protoplasma · 2014Review
- Vascular effects of exercise: endothelial adaptations beyond active muscle beds.Physiology (Bethesda, Md.) · 2011Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Our goal was to determine whether exercise training (ExT) alleviates impaired nitric oxide synthase (NOS)-dependent dilation of pial arterioles during chronic exposure to nicotine. We measured dilation of cerebral (pial) arterioles in sedentary and exercised control and nicotine-treated (2 mg·kg(-1)·day(-1) for 4 wk via an osmotic minipump) rats to an endothelial NOS (eNOS)-dependent (ADP), a neuronal NOS (nNOS)-dependent [N-methyl-D-aspartic acid (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we harvested brain tissue from sedentary and exercised control and nicotine-treated rats to measure the production of superoxide anion and measured superoxide dismutase-1 (SOD-1) protein in cerebral microvessels using Western blot. We found that eNOS-and nNOS-dependent, but not NOS-independent, vasodilation was impaired in nicotine-treated compared with control rats. In addition, the production of superoxide anion (lucigenin chemiluminescence) was increased, and SOD-1 protein decreased, in rats treated with nicotine compared with control rats. Further, although ExT did not significantly affect eNOS- or nNOS-dependent vasodilation in control rats, ExT restored impaired eNOS- and nNOS-dependent responses in nicotine-treated rats. In addition, the increase in superoxide anion production observed in nicotine-treated rats was reduced by ExT, and SOD-1 protein was increased in nicotine-treated rats by ExT. We suggest that ExT restores impaired NOS-dependent dilation of pial arterioles during chronic exposure to nicotine by a mechanism related to the formation of superoxide anion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.