The role of α-adrenergic mechanisms in sympathetic baroreflex control of human blood pressure.

This study tested the hypothesis that neural and vascular α-adrenergic mechanisms contribute to sympathetic baroreflex regulation of human blood pressure. Muscle sympathetic nerve activity (MSNA; peroneal microneurography) was measured and sympathetic action potentials (APs) were extracted from the filtered MSNA neurogram (continuous wavelet transform) in eight participants (5 females; 28±7 years) during a baseline (BSL) condition and a dexmedetomidine infusion (DEX; α-adrenergic receptor agonist; 10 min loading dose at 0.225 μg/kg; maintenance dose: 0.1-0.5 μg/kg/hr). Sympathetic AP baroreflex threshold and sensitivity gains were measured (spontaneous method). We quantified the transduction of integrated MSNA to diastolic blood pressure (DBP; signal averaging) and calculated an index of transduction gain as the slope of the relationship between maximum DBP and the number of cardiac cycles to maximum DBP. DEX reset the baroreflex operating point for medium APs to lower firing probabilities (AP cluster 4; BSL: 20±6 to DEX: 6±5 %, P<0.0004), lower DBP (72±9 to 65±10 mmHg, P<0.0001), and reduced gain (AP cluster 4: -6.5±2.0 to -2.0±0.7 %/mmHg, P<0.0001). DEX reset the AP baroreflex sensitivity operating point to fewer AP clusters/burst (3.4±0.7 to 2.9±0.8 clusters/burst, =0.0156) but did not change gain. DEX reduced DBP transduction (cardiac cycle 6: 4.3±3.2 to 3.3±2.0 mmHg, =0.0032), increased the time to peak DBP (6±1 to 11±3 cardiac cycles, =0.0054), and reduced the DBP transduction gain (0.81±0.72 to 0.36±0.37 mmHg/cardiac cycle, =0.0012). These data suggest that neural and vascular α-adrenergic mechanisms contribute to integrative sympathetic baroreflex regulation of blood pressure in humans.