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Am J Physiol Heart Circ Physiol (December 19, 2002). doi:10.1152/ajpheart.00229.2002
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Submitted on March 18, 2002
Accepted on December 17, 2002

Hypovolemia and MSNA Discharge Patterns: Assessing and Interpreting Sympathetic Responses

Derek S. Kimmerly1 and J. K. Shoemaker1*

1 School of Kinesiology, The University of Western Ontario, Neurovascular Research Laboratory, London, Ontario, Canada

* To whom correspondence should be addressed. E-mail: kshoemake{at}uwo.ca.

Previously we demonstrated that diuretic-induced hypovolemia resulted in an enhanced baroreflex-mediated increase in integrated muscle sympathetic nerve activity (MSNA) and vasomotor tone during lower body negative pressure (LBNP) (10). The purpose of this paper was to perform a retrospective analysis of these data and examine the ability of relative MSNA burst amplitude distributions to highlight differences in baseline sympathetic nerve discharge patterns. An additional purpose was to determine whether differential responses in MSNA burst frequency and amplitude affect conclusions regarding sympathetic reflex control. MSNA, stroke volume (SV, Doppler), and estimated central venous pressure (CVP, dependent arm technique) were measured during lower body negative pressure (LBNP) within placebo (NORMO) and diuretic (HYPO; spironolactone; 100 mg/day for 3 days) conditions (n=8). Compared to NORMO, MSNA burst frequency at rest was elevated and there was a rightward shift in the median of the relative burst amplitude distribution (P<0.05) in HYPO. During LBNP, the larger increase in total MSNA during HYPO vs. NORMO was due to greater increases in relative burst amplitude with no difference in the burst frequency response. The MSNA burst frequency response to LBNP was shifted to a higher position on the same MSNA - CVP curve during HYPO when compared to NORMO. In contrast, the HYPO burst amplitude response was shifted to a new curve with a slope that was similar to the NORMO relationship. The data support the use of probability distribution analysis to examine intra-individual differences in baseline and reflex-mediated increases in MSNA burst amplitude. Furthermore, the differential effect of hypovolemia on the responses of burst frequency and amplitude during graded LBNP suggests that burst frequency data alone may not adequately represent reflex control of sympathetic outflow.




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