Sympathetic vascular transduction in adults with hypertension and obesity-associated hypertension.

Half of adult Americans have high resting blood pressure (BP). Although elevated muscle sympathetic nerve activity (MSNA) is a common characteristic of essential hypertension, resting sympathetic activation is highly variable. This variability may relate to alterations in the transduction of MSNA to vasoconstriction. It is unknown if sympathetic vascular transduction is altered in hypertension, or how obesity, a common comorbidity, modifies vascular transduction. Sympathetic transduction was quantified in twelve normotensive (CON; age: 38±10 years, BMI: 25±3 kg/m2) and thirty hypertensive adults (12 non-obese [N-HTN]: age, 44±6 years, BMI: 27±3 kg/m2; and 18 with obesity [OB-HTN]: age: 40±10 years, BMI: 38±5 kg/m2). Continuous measurements of MSNA (microneurography), mean arterial pressure (MAP, photoplethysmography), and superficial femoral artery blood flow (LBF, doppler ultrasound) were used to calculate beat-by-beat leg vascular conductance (LVC; LBF/MAP). Transduction to LVC and MAP were quantified using signal averaging and compared using mixed-effects model with age, sex, race, and menopausal status as covariates. MSNA burst frequency (P=0.255) and incidence (P=0.417) were not different between groups. Sympathetic vascular transduction to multiple MSNA bursts was blunted in N-HTN (group: P=0.029), leading to a slower BP response compared to CON (interaction: P=0.030). The downregulation of sympathetic vascular transduction was less apparent in OB-HTN and associated with higher sympathetic transduction to diastolic BP compared to N-HTN (P=0.041). Compared to CON, sympathetic vascular transduction was attenuated in N-HTN but remained relatively preserved in OB-HTN. These data indicate that OB-HTN may be characterized by a greater contribution of sympathetic vascular transduction to blood pressure regulation.