Abstract
Endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization and relaxation, and endothelium-independent relaxations to the nitric oxide donor sodium nitroprusside and the adenosine 5'-triphosphate (ATP)-sensitive K(+)-channel opener levcromakalim were both impaired in mesenteric arteries of type II diabetic Goto-Kakizaki rats. The treatment with the superoxide dismutase mimetic tempol or its combination with the angiotensin II type 1 receptor blocker candesartan failed to improve EDHF-mediated responses, although both treatments partially improved endothelium-independent relaxations. These findings suggest that increased oxidative stress may in part account for the impaired endothelium-independent relaxations in diabetes, while it does not play a major role in the impaired EDHF-mediated responses.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antioxidants / metabolism
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Antioxidants / pharmacology
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Blood Pressure / drug effects
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Body Weight / drug effects
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Cyclic N-Oxides / metabolism
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Cyclic N-Oxides / pharmacology*
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Diabetes Mellitus, Experimental / drug therapy*
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Diabetes Mellitus, Experimental / physiopathology
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Diabetes Mellitus, Type 2 / drug therapy*
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Diabetes Mellitus, Type 2 / physiopathology
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Disease Models, Animal
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Endothelium, Vascular / drug effects*
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Endothelium, Vascular / physiology
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Heart Rate / drug effects
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Male
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Membrane Potentials / drug effects
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Mesenteric Arteries / drug effects
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Mesenteric Arteries / physiology
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Molecular Mimicry
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Rats
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Rats, Wistar
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Spin Labels
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Superoxide Dismutase / metabolism
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Vasodilation / drug effects*
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Vasodilation / physiology
Substances
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Antioxidants
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Cyclic N-Oxides
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Spin Labels
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Superoxide Dismutase
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tempol