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1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States
* To whom correspondence should be addressed. E-mail: rhester{at}physiology.umsmed.edu.
Individuals with Metabolic Syndrome exhibit insulin resistance and attenuated functional vasodilatory response to exercise. We have shown that impaired functional vasodilation in obese Zucker rats (OZRs) is associated with enhanced thromboxane receptor (TP)-mediated vasoconstriction. We hypothesize that insulin resistance, hyperglycemia/hyperlipidemia and the resultant reactive oxygen species (ROS) are responsible for the increased TP-mediated vasoconstriction in OZRs, resulting in an impaired functional vasodilation. Eleven week old male lean (LZRs) and obese Zucker rats were fed normal rat chow or chow containing rosiglitazone (5mg/kg/day) for 2 weeks. In another set of experiment LZRs and OZRs were treated with 2mM of TEMPOL (drinking) for 7-10 days. After the treatments, spinotrapezius muscles were prepared and the arcade arteriolar diameters were measured following muscle stimulation and AA application (10 µM) in the absence and presence of the TP antagonist SQ 29548 (1µM; SQ). OZRs exhibited higher insulin, glucose, triglycerides and superoxide levels and increased NADPH oxidase activity as compared with LZRs. Functional and AA-induced vasodilations were impaired in the OZRs. Rosiglitazone treatment improved insulin, glucose, triglycerides and superoxide levels as well as the NADHP oxidase activity in OZRs. Both rosiglitazone and TEMPOL treatment improved the vasodilatory responses in OZRs with no effect in LZRs. SQ treatment improved the vasodilatory responses in nontreated OZRs with no effect in lean or the treated OZRs. These results suggest that insulin resistance and the resultant increased ROS impair functional dilation in OZRs by increasing the TP-mediated vasoconstriction.
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