Central interleukin-1beta antibody increases renal and splenic sympathetic nerve discharge

We tested the hypothesis that intracerebroventricular (lateral ventricle) administration of interleukin-1beta (IL-1beta) antibody increases the level of sympathetic nerve discharge (SND) in alpha-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-1beta antibody (15 microg, 50 microl icv) in baroreceptor-intact (intact) and sinoaortic-denervated (SAD) rats. The following observations were made. First, intracerebroventricular infusion of IL-1beta 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-1beta antibody infusion and sympathoexcitatory responses were higher in SAD compared with intact rats. Third, intracerebroventricular administration of a single dose of IL-1beta antibody (15 microg, 5 microl 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-1beta plays a role in the tonic regulation of SND and arterial blood pressure.