| Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats. | |
| | |
MedLine Citation:
|
PMID: 21169403 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
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. |
| | |
Authors:
|
William G Mayhan; Denise M Arrick; Kaushik P Patel; Hong Sun |
Related Documents
:
|
1796783 - Fine structural aspects of postnatal development of feline lung. 18724033 - Biphasic elevation of bilirubin oxidation during myocardial ischemia reperfusion. 7936023 - Progressive decline in renal function induces a gradual decrease in total hemoglobin an... |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-12-17 |
Journal Detail:
|
Title: American journal of physiology. Heart and circulatory physiology Volume: 300 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2011 Mar |
Date Detail:
|
Created Date: 2011-03-03 Completed Date: 2011-05-26 Revised Date: 2012-03-01 |
Medline Journal Info:
|
Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
|
Languages: eng Pagination: H1013-20 Citation Subset: IM |
Affiliation:
|
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA. wgmayhan@unmc.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adenosine Diphosphate
/
pharmacology Animals Arterioles / drug effects, enzymology, physiology* Cerebral Arteries / drug effects, enzymology, physiology* Cerebral Cortex / blood supply*, chemistry, enzymology Diabetes Mellitus, Experimental / enzymology, physiopathology Diabetes Mellitus, Type 1 / enzymology, physiopathology* Male N-Methylaspartate / pharmacology Nitric Oxide Synthase / physiology* Nitroglycerin / pharmacology Physical Conditioning, Animal / physiology* Rats Rats, Sprague-Dawley Superoxides / metabolism Vasodilation / drug effects, physiology Vasodilator Agents / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
|
AA-11288/AA/NIAAA NIH HHS; HL-090657/HL/NHLBI NIH HHS; R01 HL090657-01A2/HL/NHLBI NIH HHS; R01 HL090657-02/HL/NHLBI NIH HHS; R01 HL090657-03/HL/NHLBI NIH HHS; R01 HL090657-04/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Vasodilator Agents; 11062-77-4/Superoxides; 55-63-0/Nitroglycerin; 58-64-0/Adenosine Diphosphate; 6384-92-5/N-Methylaspartate; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Functional medial thickening and folding of the internal elastic lamina in coronary spasm.
Next Document: Mthfr deficiency induces endothelial progenitor cell senescence via uncoupling of eNOS and downregul...