ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Optimizing cerebrovascular endothelial health through shear stress modulation.Experimental physiology · 2025Review
- A cannabinoid type 2 (CB2) receptor agonist augments NOS-dependent responses of cerebral arterioles during type 1 diabetes.Microvascular research · 2021Article
- Exercise training ameliorates cerebrovascular dysfunction in a murine model of Alzheimer's disease: role of the P2Y2 receptor and endoplasmic reticulum stress.American journal of physiology. Heart and circulatory physiology · 2020Article
- Cerebral vs. Cardiovascular Responses to Exercise in Type 2 Diabetic Patients.Frontiers in physiology · 2020Review
- Psychological stress-induced cerebrovascular dysfunction: the role of metabolic syndrome and exercise.Experimental physiology · 2018Article
- Impact of Metabolic Diseases on Cerebral Circulation: Structural and Functional Consequences.Comprehensive Physiology · 2018Review
- Aerobic exercise prevents rarefaction of pial collaterals and increased stroke severity that occur with aging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 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
- Vessel Dilation Attenuates Endothelial Dysfunction Following Middle Cerebral Artery Occlusion in Hyperglycemic Rats.CNS neuroscience & therapeutics · 2016Article
- Neonatal hyperglycemia induces oxidative stress in the rat brain: the role of pentose phosphate pathway enzymes and NADPH oxidase.Molecular and cellular biochemistry · 2015Article
- NADPH Oxidase Activity in Cerebral Arterioles Is a Key Mediator of Cerebral Small Vessel Disease-Implications for Prevention.Healthcare (Basel, Switzerland) · 2015Review
- Modulation of angiotensin II signaling following exercise training in heart failure.American journal of physiology. Heart and circulatory physiology · 2015Review
- Central mechanisms for exercise training-induced reduction in sympatho-excitation in chronic heart failure.Autonomic neuroscience : basic & clinical · 2015Review
- Physical exercise associated with NO production: signaling pathways and significance in health and disease.Frontiers in cell and developmental biology · 2015Review
- Effects of aerobic exercise training on large-conductance Ca(2+)-activated K (+) channels in rat cerebral artery smooth muscle cells.European journal of applied physiology · 2013Article
- Article
- Influence of exercise training on ischemic brain injury in type 1 diabetic rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Organ-based response to exercise in type 1 diabetes.ISRN endocrinology · 2012Article
- Vascular effects of exercise: endothelial adaptations beyond active muscle beds.Physiology (Bethesda, Md.) · 2011Review
- Exercise increases insulin content and basal secretion in pancreatic islets in type 1 diabetic mice.Experimental diabetes research · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we measured superoxide anion levels in brain tissue under basal conditions in sedentary and exercised nondiabetic and diabetic rats. Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. We found that ADP and NMDA produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic rats. In contrast, ADP and NMDA produced only minimal vasodilation in sedentary diabetic rats. ExT restored impaired ADP- and NMDA-induced vasodilation observed in diabetic rats to that observed in nondiabetics. Nitroglycerin produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic and diabetic rats. Superoxide levels in cortex tissue were similar in sedentary and exercised nondiabetic rats, were increased in sedentary diabetic rats, and were normalized by ExT in diabetic rats. Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D.
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