Interleukin–1β (IL-1β) receptors are abundantly expressed in brain stem regions involved in respiratory control. We hypothesized that systemic administration of IL-1β would increase ventilation (VE ), and that nitric oxide, eicosanoids, and glucocorticoid receptors would modulate IL-1β-induced cardioventilatory responses. Intravenous injections of three doses (37.5 ng kg-1, 75 ng kg-1 and 150 ng kg-1) of IL-1b induced monophasic increases in (VE), heart rate (HR), and blood pressure (BP) which had a distinctly different onset and duration of action compared to IL-1β-induced body temperature elevations. Pre-treatment with the nitric oxide inhibitor L-NAME was associated with decreased peak VE responses, without affecting the latency and duration of IL-1β. L-NAME also enhanced HR responses while pressor responses were attenuated. Eicosanoid inhibition with indomethacin resulted in markedly attenuated V responses. However, cardiovascular responses to IL-1β were not modified by indomethacin. In contrast, pre-treatment with dexamethasone, was not associated with any changes in the IL-1β-induced VE, HR, or BP responses. We conclude that IL-1β increases of VE are dose-dependent and are not time-locked with the pyrexic response suggesting the possibility that distinct neural pathways may underlie these responses. In addition, nitric oxide and eicosanoid-dependent mechanisms modulate IL-1β ventilatory effects. [ABSTRACT FROM AUTHOR]
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