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Preserved β-adrenergic mediated vasodilation in skeletal muscle of young obese adults despite shifts in cyclooxygenase and nitric oxide synthase.

Central adiposity is associated with greater sympathetic support of blood pressure. β-adrenergic receptors (β-AR) buffer sympathetically-mediated vasoconstriction and β-AR mediated vasodilation is attenuated in preclinical models of obesity. With this information, we hypothesized β-AR vasodilation would be lower in obese compared to normal weight adults. Because β-AR vasodilation in normal weight adults is limited by cyclooxygenase (COX) restraint of nitric oxide synthase (NOS), we further explored the contributions of COX and NOS to β-AR vasodilation in this cohort.


METHODS
Forearm blood flow (FBF, Doppler ultrasound) and mean arterial blood pressure (MAP, brachial arterial catheter) were measured and forearm vascular conductance was calculated (FVC=FBF/MAP). The rise in FVC from baseline (ΔFVC) was quantified during graded brachial artery infusion of Isoproterenol (ISO, 1-12 ng/100g/min) in normal weight (n=36) and obese (n=22) adults (18-40 years old). In a subset of participants, ISO-mediated vasodilation was examined prior to and during inhibition of NOS (L-NMMA), COX (Ketorolac), and NOS + COX (L-NMMA + Ketorolac).


RESULTS
ISO-mediated increases in FVC did not differ between groups (p=0.57). L-NMMA attenuated ISO-mediated ΔFVC in normal weight (p=0.03) but not obese (p=0.27) adults. In normal weight adults, Ketorolac increased ISO-mediated ΔFVC (p<0.01) and this response was lost with concurrent L-NMMA (p=0.67). In contrast, neither Ketorolac (p=0.81) nor Ketorolac + L-NMMA (p=0.40) altered ISO-mediated ΔFVC in obese adults.


CONCLUSION
Despite shifts in COX and NOS, β-AR vasodilation is preserved in young obese adults. These data highlight the presence of a compensatory shift in microvascular control mechanisms in younger obese humans.