Role of vascular adrenergic receptors in mediating beat-by-beat sympathetic vascular transduction in young females

Introduction: Sympathetic vascular transduction represents beat-to-beat reductions in limb vascular conductance following bursts of sympathetic nerve activity and is mediated by α-adrenergic receptors (AR) in young males. Greater β-AR sensitivity and lower α-AR sensitivity in young females affords potential female-specific adrenergic mediation of sympathetic vascular transduction that remain untested. We aimed to determine the roles of β- and α-AR on beat-to-beat sympathetic vascular transduction at rest in young females. We hypothesized sympathetic vascular transduction would be 1) augmented under β-AR blockade and 2) attenuated under α-AR blockade in young females. Methods: Six premenopausal females (assigned at birth; 29±11 yrs; 25±3 kg/m 2 ; early follicular phase) were instrumented supine for beat-to-beat measures of mean arterial pressure (MAP, finger plethysmography), femoral artery blood flow (FBF, duplex Doppler ultrasound), and muscle sympathetic nerve activity (MSNA, peroneal microneurography). Participants completed three 10-min conditions: 1) baseline, 2) β-AR blockade (intravenous propranolol, 0.0040 mg/kg/min), and 3) combined β- and α-AR blockade (intravenous propranolol + phentolamine, 0.01428 mg/kg/min). Spike-triggered signal averaging characterized beat-to-beat changes in MAP and femoral vascular conductance (FVC=FBF/MAP) for 15 cardiac cycles following each burst of MSNA. Peak (MAP) and nadir (FVC) percent changes were also calculated. Results: MAP increased (P< 0.001) following MSNA bursts at baseline, reaching a peak in the 5th cardiac cycle (+2±1%, Tukey P< 0.001), and FVC decreased (P< 0.001), reaching a nadir in the 8th cardiac cycle (-12±4%, Tukey P< 0.001). Under β-AR blockade, MAP similarly peaked in the 5th cardiac cycle (+2±1%, Tukey P< 0.001) and FVC reached a nadir in the 8th cardiac cycle (-14±5%, Tukey P< 0.001). Under combined β+α-AR blockade, MAP peaked in the 9th cardiac cycle (+1±1%, Tukey P=0.007), but FVC did not significantly change following MSNA bursts (P=0.719). Peak %ΔMAP (P=0.007) was significantly attenuated under combined β+α-AR blockade (+1±1%) vs. baseline (+2±1%, Tukey P=0.024) with no difference between baseline and β-AR blockade (+3±1%, Tukey P=0.789). Nadir %ΔFVC (P< 0.001) was significantly attenuated under combined β+α-AR blockade (-8±6 vs. -18±8% at baseline, Tukey P=0.001) with no effect of β-AR blockade (-18±6%, Tukey P=0.989). Conclusions: These preliminary results show α-AR blockade attenuates beat-to-beat sympathetic vascular transduction at rest in young females. In contrast, β-AR blockade does not alter beat-to-beat sympathetic vascular transduction. Present findings diverge from prior evidence supporting β-AR-mediated blunting of sympathetic blood pressure transduction in young females derived from linear regression analysis. Differences in study findings may be related to differing methodological and analytical approaches to quantify sympathetic transduction. Current data support key α-AR, but not β-AR, contributions to sympathetic-mediated beat-to-beat regulation of vascular tone and blood pressure in healthy young females. Funding: American Heart Association (NGB 25POST1362901; JKL 24TPA1300511) and NextGen Precision Health Postdoctoral Fellowship (NGB). This abstract was presented at the American Physiology Summit 2026 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.