Muscle Sympathetic Nerve Activity During a Sodium and Volume Load

Abstract

Animal models demonstrate a strong association between plasma osmolality and sympathetic outflow. The purpose of this study was to determine if a stepwise increase in plasma osmolality causes parallel increases in blood pressure and muscle sympathetic nerve activity. Eight healthy, normotensive subjects (24±2 years) completed both a 60-minute hypertonic (3% NaCl; HSI) and normal (0.9% NaCl; NSI) saline infusion (0.15ml/kg/min) at random separated by one month. Heart rate (ECG), mean arterial pressure (Finometer; MAP) and muscle sympathetic nerve activity (MSNA) were assessed at baseline, 20, 40, and 60 minutes. Sodium, osmolality, and hematocrit (Hct) were assessed throughout the infusion. A 2-way repeated measures ANOVA was used to determine statistical significance. Results are reported as mean±SE. Osmolality increased during the HSI (pre=289±1, post=297±1 mOsm/kg; p<0.03) but not during the NSI (pre=290±1, post=290±1 mOsm/kg; p>0.40). Hct declined during the HSI (42±1 to 37±1%) and the NSI (41±1 to 39±1%). There was a time and treatment interaction for burst frequency (p=0.03): burst frequency initially increased from 15±3 to 19±2 during the HSI, and declined from 14±3 to 12±2 bursts/min during the NSI (post hoc at the 20-minute time point; p<0.01) before returning to baseline values. There was a time (p=0.003) but no treatment effect for MAP. Preliminary results suggest that increases in osmolality may cause acute increases in MSNA in humans. Supported by NIH grant R15 HL074851-01