Humoral influences on resting and baroreflex control of sympathetic neural activity

Previous studies have shown that arginine vasopressin (AVP) is tightly linked to osmolality in humans. Additionally, hyperosmolality has been shown to increase sensitivity of baroreflex control of muscle sympathetic nerve activity (MSNA). In our previous study, volume depletion without changes in osmolality was associated with increased MSNA with unchanged baroreflex sensitivity (BRS) and AngII appeared to mediate these changes. We therefore hypothesized that among euhydrated individuals, (1) Ang II would not be related to osmolality but would linearly correlate with CVP and MSNA and (2) positive relationships would exist between osmolality and AVP, and between AVP and MSNA BRS. Subjects were instrumented with ECG, peripherally inserted central catheter for central venous pressure (CVP) measurement and blood draws, peroneal microneurography for MSNA and Finometer for continuous blood pressure. Data were recorded during baseline and during transient changes in blood pressure elicited by nitroprusside and phenylephrine (modified Oxford technique). Interindividual relationships were studied between humoral substances (AVP and AngII) and osmolality, MSNA and sensitivity of baroreflex control of MSNA by Pearson's correlation. Osmolality and AVP were moderately related (r=0.61, P < 0.05) and there was no correlation between CVP and AVP (r=0.1). AVP and MSNA BRS showed a negative correlation (r=−0.67), whereas AngII showed a moderate negative association with CVP (r=−0.49) and did not correlate with osmolality (r=−0.07). However, AngII had a moderate negative association with resting MSNA (r=−0.55, P < 0.05). Our findings suggest that AVP, under control of osmolality, may exert important regulatory influences on MSNA via the baroreflex. Supported by AHA 0750036Z.