The effect of IL-1 beta and TNF alpha infused into nucleus tractus solitari(NTS), nucleus parabrachialis medialis (NPBmed) and third cerebral ventricle ofnormotensive rats on blood pressure (BP) and heart rate (HR) was investigated.Microinfusion of IL-1 beta and TNF alpha into the third cerebral ventricle andNPBmed of normotensive rats produced a dose-dependent hypotensive and bradycardicresponse. A similar cardiovascular response was produced by infusion of IL1 beta into NTS but not by TNF alpha. When rats were pre-treated with Escherichia colilipopolisaccharide (LPS), an enhancement of cardiovascular response elicited byIL-1 beta and TNF alpha was found. Thus, IL-1 beta and TNF alpha producecardiovascular responses when infused into specific areas of the CNS. This effectis potentiated by LPS and this may explain the alteration in cardiovascularregulation which can be observed in diseases in which an excess of circulatingendotoxins and cytokines may occur.

Central cardiovascular responses induced by interleukin 1β and tumor necrosis factor α infused into nucleus tractus solitarii, nucleus parabrachialis medialis and third cerebral ventricle of normotensive rats

Muscoli C;Palma E;
2001-01-01

Abstract

The effect of IL-1 beta and TNF alpha infused into nucleus tractus solitari(NTS), nucleus parabrachialis medialis (NPBmed) and third cerebral ventricle ofnormotensive rats on blood pressure (BP) and heart rate (HR) was investigated.Microinfusion of IL-1 beta and TNF alpha into the third cerebral ventricle andNPBmed of normotensive rats produced a dose-dependent hypotensive and bradycardicresponse. A similar cardiovascular response was produced by infusion of IL1 beta into NTS but not by TNF alpha. When rats were pre-treated with Escherichia colilipopolisaccharide (LPS), an enhancement of cardiovascular response elicited byIL-1 beta and TNF alpha was found. Thus, IL-1 beta and TNF alpha producecardiovascular responses when infused into specific areas of the CNS. This effectis potentiated by LPS and this may explain the alteration in cardiovascularregulation which can be observed in diseases in which an excess of circulatingendotoxins and cytokines may occur.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12317/8135
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