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Prostaglandin‐Mediated Vasodilation in Metabolic Syndrome: Role of Oxidative Stress

Prostaglandin‐mediated vasodilation in metabolic syndrome (MetS) may be influenced by an excess of reactive oxygen species (ROS). We hypothesized vasodilatory responses to prostacyclin (PGI2) would be reduced in adults with MetS compared to lean adults, and acute ROS scavenging with ascorbic acid (AA) would restore vasodilation in MetS. Forearm blood flow (FBF, Doppler Ultrasound) was measured in younger (19–53 yrs) lean controls (n=6, BMI=23±1 kg.m−2) and adults with MetS (n=11, BMI=38±2). A brachial artery cathether was inserted for blood pressure (BP) measurement and local drug infusion. Responses to the PGI2 analog epoprostenol (PGI2, 10 ug.dL−1.min−1) were measured before and during AA infusion. Vasodilatory responses were assessed as relative forearm vascular conductance (rFVC = FBF.BP−1.dL−1) to account for group differences in BP and forearm size. rFVC responses to PGI2 were lower in MetS when compared to lean controls (p<0.01). Plasma total antioxidant capacity increased with AA infusion in both groups (p<0.05). The change in rFVC with AA infusion was not significant in either group (Lean p=0.09, MetS p=0.06). These results indicate PGI2‐mediated vasodilation is reduced in MetS, but this reduction is unlikely due to increased ROS. Support: NIH HL091397 and APS Undergraduate fellowship