Impact of Adiposity on Vascular Adrenergic Receptor Sensitivity in Young Males and Females

Introduction: Obesity increases the risk of hypertension, however conflicting studies examining the role of adiposity on underlying neurovascular control mechanisms are limited by mixed-sex cohorts. Normal weight males exhibit greater α-adrenergic receptor (AR) mediated vasoconstriction and lower β-AR mediated vasodilation compared to females, supporting an important role for sex in neurovascular control. We sought to examine the impact of adiposity on α-AR vasoconstriction and β-AR vasodilation in separate cohorts of males and females. We hypothesized greater adiposity would be associated with greater α-AR vasoconstriction and lower β-AR vasodilation in males and females. Methods: Twenty-four young adults (12F, 25­±7 yrs, 24±3 kg/m 2 ; 12M, 29±6 yrs, 25±2 kg/m 2 ) were instrumented for measurement of forearm blood flow (FBF, venous occlusion plethysmography) and underwent brachial artery catheterization for local drug infusion and blood pressure (BP) monitoring. Isoproterenol (non-specific β-AR agonist) was infused (12 ng/dL/min) to assess β-AR vasodilation. Following β-AR blockade (propranolol, 25 mcg/dL/min), norepinephrine was infused (8 ng/dL/min) to assess α-AR vasoconstriction. Forearm vascular conductance was calculated (FVC=FBF/mean BP) and reported as the relative change from baseline during infusions (%ΔFVC). Pearson r correlations assessed associations between %ΔFVC and indices of adiposity [body mass index (BMI), waist circumference, percent body fat (dual energy x-ray absorptiometry), and android: gynoid fat ratio (A:G ratio)]. Results: In females, α-AR vasoconstriction ( i.e., decreasing %ΔFVC) was negatively associated with BMI ( r =-0.670, p =0.017), waist circumference ( r =-0.666, p =0.018), and A:G ratio ( r =-0.583, p =0.047), but not total body fat ( p =0.207), demonstrating greater α-AR vasoconstriction with increased central adiposity in females. No significant associations between α-AR vasoconstriction and indices of adiposity were observed in males (all p ≥0.240). β-AR vasodilation was not associated with BMI, waist circumference, A:G ratio or total body fat in males (all p ≥0.313) nor females (all p ≥0.068). Conclusion: These preliminary data show α-AR vasoconstriction is exacerbated by increasing central adiposity in females independent of total body fat. In contrast, β-AR vasodilation is not associated with adiposity in males nor females. Implications include sex-specific and adiposity-mediated mechanisms of vascular adrenergic function that may impact chronic conditions predominantly affecting young females with obesity ( e.g., polycystic ovarian syndrome). Funding: National Institutes of Health (1R01HL153523), MizzouForward, Mizzou Research Excellence Program. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.