Limited Effect of Systemic β-Blockade on Sympathetic Outflow

Abstract

Central β-adrenoreceptors may augment sympathetic outflow. We tested the hypothesis that β-blockade attenuates central sympathetic outflow by inhibiting central adrenoreceptors. We studied 18 healthy controls (4 female, 14 male; age, 26±6 years, body mass index, 23±3 kg/m 2 ). ECG, brachial, and finger arterial blood pressure, muscle sympathetic nerve activity, and respiration were measured continuously before and during complete β-blockade. Subjects received a total intravenous dose of 0.21 mg/kg of propranolol in 15 minutes. Spontaneous baroreflex slopes were calculated using the sequence technique (BRSup, BRSdown). The sympathetic baroreflex slope was determined at baseline using phenylephrine and sodium nitroprusside infusions. The subjects underwent cold pressor testing before and during β-blockade. The R-R interval increased from 861±119 ms at baseline to 952±141 ms during β-blockade ( P <0.01). Blood pressure was 117±9/65±8 mm Hg at baseline and 117±10/67±8 mm Hg during β-Blockade ( P =NS). β-Blockade did not affect baroreflex sensitivity (BRSup: 21±10 versus 28±11 ms/mmHg, P <0.1; BRSdown: 17±8 versus 20±8 ms/mmHg, P =NS). Muscle sympathetic nerve activity increased significantly during β-blockade (number of bursts/100 beats: 32±9 versus 40±14, P <0.05), compared with baseline. However, the operating points of the parasympathetic and sympathetic baroreflex during β-blockade were on the baroreflex curves obtained at baseline. β-Blockade blunted the heart rate response to cold pressor testing; blood pressure and muscle sympathetic nerve activity responses were similar. Our study demonstrates that propranolol does not cause an acute decrease in sympathetic activity in normotensive young subjects. This, observation is not consistent with an important tonic stimulatory effect of β-adrenoreceptors in the brain.