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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Biomedical Sciences, Grand Valley State University, Allendale, MI, USA
3 Department of Physiology and Pharmacology, West Virginia University School of Medicine, Morgantown, WV, USA
* To whom correspondence should be addressed. E-mail: jfrisbee{at}hsc.wvu.edu.
This study tested the hypothesis that evolution of the metabolic syndrome in obese Zucker rats (OZR) leads to impaired dilator reactivity of cerebral resistance arteries vs. responses determined in lean Zucker rats (LZR). Middle cerebral arteries (MCA) from 17-week old male LZR and OZR were isolated and cannulated with glass micropipettes. Vascular reactivity was assessed in response to challenge with acetylcholine (Ach), sodium nitroprusside (SNP), reductions and elevations in PO2, 5-hydroxytryptamine (5-HT), and increased intralumenal pressure. Vessels were treated with the free radical scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL) to assess the role of superoxide production in altering reactivity, and passive vascular wall mechanics were assessed in each vessel. Vascular superoxide production was assessed in isolated arteries using fluorescence microscopy. Vessel dilation to Ach and hypoxia was impaired in OZR vs. LZR, although responses to SNP were normal. Vessel constriction to 5-HT, elevated PO2, and elevated intralumenal pressure was enhanced in OZR vs. LZR. Fluorescence microscopy demonstrated an increased superoxide production in arteries of OZR vs. LZR, correctable by incubation with TEMPOL. While treatment of vessels from OZR with TEMPOL improved dilation to Ach and hypoxia, constrictor responses to 5-HT, elevated PO2 and pressure were not altered by TEMPOL treatment. Indices of vessel wall mechanics were comparable between groups. These results suggest that vasodilator reactivity of MCA of OZR in response to endothelium-dependent dilator stimuli is impaired vs. LZR and that this may represent a reduced bioavailability of signaling molecules due to oxidant scavenging. However, oxidative stress-independent increases in myogenic tone and constrictor reactivity may contribute to blunted dilator responses of cerebral microvessels.
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