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Stress‐mediated increases in endothelial NO are abolished in diabetic female rats
Endothelial dysfunction occurs early in human and animal models of diabetes. Chronic stress (CS) is considered a co‐morbidity factor in diabetic humans. We hypothesize that CS adds to endothelial dysfunction in the diabetic milieu. Our objective was to examine endothelial associated vascular changes...
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Published in: | The FASEB journal 2007, Vol.21 (6), p.A904-A904 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Endothelial dysfunction occurs early in human and animal models of diabetes. Chronic stress (CS) is considered a co‐morbidity factor in diabetic humans. We hypothesize that CS adds to endothelial dysfunction in the diabetic milieu. Our objective was to examine endothelial associated vascular changes during CS and early diabetes. After 6 wks of treatment, adult female control and STZ injected SD rats were exposed to 2 hr cold stress daily for 2 wks. 2nd generation mesenteric arterioles were assayed in a wire myograph for response to acetylcholine (ACh), and phenylephrine (PE) with and without L‐NAME, which inhibits constitutive NO production and increases PE sensitivity. In normal controls, L‐NAME increased sensitivity to PE 7‐fold (p |
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ISSN: | 0892-6638 1530-6860 |
DOI: | 10.1096/fasebj.21.6.A904-a |