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1 Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA
* To whom correspondence should be addressed. E-mail: rhester{at}physiology.umsmed.edu.
These studies tested the hypothesis that in obese Zucker rats (OZRs), a model of metabolic syndrome, the impaired functional vasodilation is due to increased thromboxane receptor(TP)-mediated vasoconstriction and/or decreased prostacyclin-induced vasodilation. Spinotrapezius arcade arterioles from 12 week old lean (LZR) and obese rats were chosen for microcirculatory observation. Arteriolar diameter (6 lean and 5 obese) was measured following 2 minutes of muscle stimulation in the absence and presence of 1µM SQ29548 (TP antagonist). Additionally, arteriolar diameter (6 for each group) was measured following application of iloprost (prostacyclin analog, 0.28µM, 2.8µM and 28µM), arachidonic acid (AA; 10µM) and sodium nitroprusside (SNP; 0.1µM, 1µM and 10µM) in the absence and presence of 1µM SQ29548. 10µM adenosine was used to induce a maximal dilation. Basal diameters were not different between LZRs and OZRs. Functional hyperemia and AA-mediated vasodilations were significantly attenuated in OZR as compared to the LZR, and treatment with 1µM SQ29548 significantly enhanced the dilations in OZRs while having no effect in LZRs. Vasodilatory responses to iloprost and SNP (1µM and 10µM) were significantly reduced in OZR. Adenosine mediated vasodilation was not different between groups. These results suggest that the impaired functional dilation in the OZR is due to an increased TP-mediated vasoconstriction and a decreased PGI2-induced vasodilation.
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