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1 Department of Veterans Affairs, Iowa City, Iowa, United States; Internal Medicine, University of Iowa, Iowa City, Iowa, United States
2 Department of Veterans Affairs, Iowa City, Iowa, United States
3 Internal Medicine, University of Iowa, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: christine-oltman{at}uiowa.edu.
We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and ZDF rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study whereas values were increased in Zucker obese rats later in the study. (TBARS: 0.45 ± 0.02, 0.59 ± 0.03* and 0.58 ± 0.03* mg/ml in serum from 28-40 week lean, Zucker obese and ZDF rats respectively). Acetylcholine (ACh) induced relaxation was not altered in vessels from lean animals from 8-40 weeks. ACh induced relaxation was nearly abolished in coronary arteries from 28-36 week old Zucker obese and by 16-36 weeks in ZDF rats, and was attenuated in aorta and mesenteric vessels from ZDF rats (% Relaxation to 10 µM Ach: 72.2±7.1. 17.9±5.9*, and 23.0±4.5* in coronary, and 67.9±9.2, 50.1±5.5 and 42.3±4.7* in mesenteric vessels from 28-40 week old lean, Zucker obese and ZDF rats respectively.) The attenuated Ach-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside induced relaxation was not altered in aorta or coronary arteries, and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
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