Lipopolysaccharide-induced hypotension is mediated by a neural pathway involving the vagus nerve, the nucleus tractus solitarius and alpha-adrenergic receptors in the preoptic anterior hypothalamic area

Abstract We recently reported that the preoptic anterior hypothalamic area (POA) mediates the hypotensive response evoked by lipopolysaccharide (LPS). In this study, we investigated how the inflammatory signal induced by LPS reaches the POA. Subdiaphragmatic vagotomy and abdominal perivagal lidocain...

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Bibliographic Details
Published in:Journal of neuroimmunology 2008-10, Vol.203 (1), p.39-49
Main Authors: Yilmaz, M. Sertac, Goktalay, Gokhan, Millington, William R, Myer, Brian S, Cutrera, Rodolfo A, Feleder, Carlos
Format: Article
Language:English
Subjects:
Acute Disease
Adrenergic alpha-Antagonists - pharmacology
Allergy and Immunology
Alpha-adrenergic receptors
Anesthetics, Local - pharmacology
Animals
Endotoxic shock
Hypotension
Hypotension - chemically induced
Hypotension - immunology
Hypotension - physiopathology
Lidocaine - pharmacology
Lipopolysaccharides - pharmacology
Male
Neurology
Nucleus tractus solitarius
Phentolamine - pharmacology
Preoptic Area - drug effects
Preoptic Area - physiopathology
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha - metabolism
Shock, Septic - chemically induced
Shock, Septic - immunology
Shock, Septic - physiopathology
Signal Transduction - immunology
Solitary Nucleus - physiopathology
Vagotomy
Vagus nerve
Vagus Nerve - drug effects
Vagus Nerve - physiopathology
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Summary:Abstract We recently reported that the preoptic anterior hypothalamic area (POA) mediates the hypotensive response evoked by lipopolysaccharide (LPS). In this study, we investigated how the inflammatory signal induced by LPS reaches the POA. Subdiaphragmatic vagotomy and abdominal perivagal lidocaine administration, or lidocaine injection into the nucleus tractus solitarius (NTS) prevented LPS hypotension. Microinjection of the alpha-adrenergic receptor antagonist phentolamine into the POA, blocked initiation of the hypotensive response and prevented the late decompensatory phase. These data suggest that LPS hypotension is mediated by the vagus nerve which conveys the signal to the NTS and, in turn, stimulates norepinephrine release within the POA.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2008.06.023