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antibody increases renal and splenic
sympathetic nerve discharge
Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506
We tested the hypothesis that
intracerebroventricular (lateral ventricle) administration of
interleukin-1
(IL-1
) antibody increases the level of sympathetic
nerve discharge (SND) in
-chloralose-anesthetized rats. Mean
arterial pressure (MAP), heart rate (HR), and SND (splenic and renal)
were recorded before (Preinfusion), during (25 min), and for 45 min
after infusion of IL-1
antibody (15 µg, 50 µl icv) in
baroreceptor-intact (intact) and sinoaortic-denervated (SAD) rats. The
following observations were made. First, intracerebroventricular infusion of IL-1
antibody (but not saline and IgG) significantly increased MAP and the pressor response was higher in SAD compared with
intact rats. Second, renal and splenic SND were significantly increased
during and after intracerebroventricular IL-1
antibody infusion and
sympathoexcitatory responses were higher in SAD compared with intact
rats. Third, intracerebroventricular administration of a single dose of
IL-1
antibody (15 µg, 5 µl for 2 min) significantly increased
splenic and renal SND in intact rats. These results suggest that under
the conditions of the present experiments central neural IL-1
plays
a role in the tonic regulation of SND and arterial blood pressure.
intracerebroventricular; sympathetic nerve activity; arterial pressure; chloralose anesthesia
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