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Am J Physiol Regul Integr Comp Physiol 297: R665-R674, 2009. First published June 17, 2009; doi:10.1152/ajpregu.00191.2009
0363-6119/09 $8.00
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ARTICLES

Discharge properties of cardiac and renal sympathetic nerves and their impaired responses to changes in blood volume in heart failure

R. Ramchandra, S. G. Hood, R. Frithiof, and C. N. May

Howard Florey Institute, University of Melbourne, Parkville, Australia

Submitted 2 April 2009 ; accepted in final form 13 June 2009

Sympathetic nerve activity (SNA) consists of discharges that vary in amplitude and frequency, reflecting the level of recruitment of nerve fibers and the rhythmic generation and entrainment of activity by the central nervous system. It is unknown whether selective changes in these amplitude and frequency components account for organ-specific changes in SNA in response to alterations in blood volume or for the impaired SNA responses to volume changes in heart failure (HF). To address these questions, we measured cardiac SNA (CSNA) and renal SNA (RSNA) simultaneously in conscious, normal sheep and sheep in HF induced by rapid ventricular pacing. Volume expansion decreased CSNA (–62 ± 10%, P < 0.05) and RSNA (–59 ± 10%, P < 0.05) equally (n = 6). CSNA decreased as a result of a reduction in burst frequency, whereas RSNA fell because of falls in burst frequency and amplitude. Hemorrhage increased CSNA (+74 ± 9%, P < 0.05) more than RSNA (+21 ± 5%, P < 0.09), in both cases because of increased burst frequency, whereas burst amplitude decreased. In HF, burst frequency of CSNA (from 26 ± 3 to 75 ± 3 bursts/min) increased more than that of RSNA (from 63 ± 4 to 79 ± 4 bursts/min). In HF, volume expansion caused no change in CSNA and an attenuated decrease in RSNA, due entirely to decreased burst amplitude. Hemorrhage did not significantly increase SNA in either nerve in HF. These findings support the concept that the number of sympathetic fibers recruited and their firing frequency are controlled independently. Furthermore, afferent stimuli, such as changes in blood volume, cause organ-specific responses in each of these components, which are also selectively altered in HF.

differential control of sympathetic nerve activity; burst amplitude; burst frequency; burst incidence; hemorrhage



Address for reprint requests and other correspondence: C. N. May, Howard Florey Institute, Univ. of Melbourne, Parkville, Victoria 3010, Australia (e-mail: clive.may{at}florey.edu.au)







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