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AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 5 1264-R1269, Copyright © 1996 by American Physiological Society
ARTICLES |
D. E. Claassen, D. A. Morgan, T. Hirai and M. J. Kenney
Department of Anatomy and Physiology, Kansas State University, Manhattan 66506, USA.
We tested the hypothesis that sustained increases in mean arterial pressure (MAP) produce nonuniform changes in regional sympathetic nerve discharges (SND) after the return of MAP to control levels. Renal, adrenal, splanchnic, and lumbar SND were recorded before, during, and after a 30-min elevation in MAP produced by phenylephrine (PE) infusion in alpha-chloralose-anesthetized spontaneously hypertensive (SH) rats. SND remained reduced from control values after PE infusion, despite the return of MAP to control levels. Importantly, the duration of poststimulus sympathoinhibition was significantly less in adrenal and splanchnic SND compared with renal and lumbar SND. In sinoaortic-denervated SH rats, SND remained at control levels during and after PE infusion. Simultaneous recordings of aortic depressor nerve (ADN) activity and SND demonstrated that prolonged renal and lumbar sympathoinhibition occurred even when ADN activity fell below control levels after PE infusion. We conclude that poststimulus responses of efferent SND in SH rats are regionally nonuniform and that renal and lumbar sympathoinhibitory responses are not mediated solely by prolonged increases in afferent baroreceptor nerve activity.
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