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1 Department of Physiology, University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: s.malpas{at}auckland.ac.nz.
We have explored the possibility that renal sympathetic nerve activity and vasomotor sympathetic nerve activity are differentially regulated. We measured sympathetic nerve activity (SNA) to the kidney and the hind limb vasculature in 7 conscious rabbits 6-8 days after the implantation of recording electrodes. Acute infusion of L-NAME (6mg/kg/min for 5 min) led to an increase in blood pressure (from 66 ± 1 mmHg to 82 ± 3 mmHg) and a decrease in heart rate (from 214 ± 15 bpm to 160 ± 13 bpm). L-NAME administration caused a significantly greater decrease in renal SNA than lumbar SNA (to 68 ± 14 % vs. 84 ± 4 % of control values respectively). Volume expansion (1.5ml/kg/min) resulted in a significant decrease in renal SNA to 66 ± 7% of control levels but no change in lumbar SNA (127 ± 20%). There was no difference in the gain of the baroreflex curves between the lumbar and renal SNA (maximum gain of -7.6 ± 0.4 n.u/mmHg for lumbar SNA vs. -7.9 ± 0.75 n.u/mmHg for renal SNA). A hypoxic stimulus (10% O2 and 3% CO2) led to identical increases in both renal and lumbar SNA (195 ± 40 % and 158 ± 21 % of control values respectively). Our results indicate tailored differential control of renal and lumbar SNA in response to acute stimuli.
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