FRUCTOSE PERFUSION IN RAT MESENTERIC ARTERIES IMPAIRS ENDOTHELIUM-DEPENDENT VASODILATION |
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| Institution: | 1. Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK;2. Radboud Institute for Health Sciences, Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;3. Unilever Research & Development, Olivier van Noortlaan 120, 3133 AT Vlaardingen, The Netherlands;4. School of Sport Science, Exercise and Health, The University of Western Australia, Crawley, Western Australia 6009, Australia;1. Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China;2. Institute of Nano Biomedicine and Engineering, Department of Instrument Science and Engineering, School of Electronic Information and Electrical Engineering, Shanghai Jiao Tong University, Shanghai, PR China;3. Shanghai Engineering Research Center for Intelligent Diagnosis and Treatment Instrument, Shanghai, PR China;4. School of Biomedical Engineering, Institute for Personalized Medicine, Shanghai Jiao Tong University, Shanghai, PR China;1. Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA;2. Institute of Biochemistry, Biological Research Center, Hungarian Academy of Sciences, Szeged, Hungary;3. Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and University of Texas Southwestern Medical Center, Dallas, TX, USA;4. Department of Kinesiology, Texas Woman’s University, Denton, TX, USA;5. Department of Pathology, Wake Forest School of Medicine, Winston–Salem, NC, USA |
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| Abstract: | We demonstrated that the fructose-induced hypertensive rat, representative of the principal metabolic abnormalities found in a majority of hypertensive patients, i.e. hypertriglyceridemia, hyperinsulinemia and insulin resistance (Syndrome X), is associated with an impaired response to endothelium-dependent vasodilators and that fructose may directly contribute to this impairment. Twelve male Wistar rats were divided into two groups, one given 10% fructose (n=6); the other no fructose (n=6) for 40 days in the drinking water. Systolic blood pressure was measured via the tail cuff method. Perfusion pressure responses to acetylcholine, were measured in the isolated perfused mesenteric vascular bed. Constrictor or dilator responses were measured as increases or decreases, respectively, of the perfusion pressure at a constant flow (4 ml/min). Fructose-fed rats had significantly higher blood pressure, insulin and triglyceride levels than control animals. In phenylephrine constricted beds, the endothelium-dependent dilatation to acetylcholine (0.001 to 1 μmol) was attenuated in the fructose-fed group compared to control animals. Whether this abnormality results from the syndromes (hyperinsulinemia, hypertension and hypertriglyceridemia) associated with the fructose-fed animal model is unknown. We therefore hypothesized that fructose can impair the endothelium-dependent vasodilator response. This was evaluated by perfusing mesenteric arteries from normal rats with control mannitol (40 mM) or fructose (40 mM). Endothelium-dependent dilation to acetylcholine was impaired in fructose-perfused mesenteric arteries. Indomethacin restored the vasodilator response to acetylcholine, suggesting that a cyclooxygenase derivative mediates the impaired response. Thus, we conclude that fructose can contribute to the impaired endothelium-dependent response in the fructose-induced hypertensive rat model. Published by Elsevier Science Inc. |
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