title: Effect of lipopolysaccharide treatment on neurogenic contraction and noradrenaline release in rat arteries.
abstract: In the present study, contractile responses and [3H]-noradrenaline overflow evoked by electrical field stimulation were assessed, respectively, in the small mesenteric artery and in tail artery removed from rats pre-treated with either saline or lipopolysaccharide (LPS). In small mesenteric arteries, LPS treatment did not significantly modify the contractile responses elicited by electrical stimulation, in the absence or in the presence of L-arginine. However, in arteries removed from rats treated with LPS, L-arginine addition produced relaxation of vessels pre-contracted with noradrenaline. The amplification of neurogenic contraction by the nitric oxide (NO) synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) was similar in arteries removed from saline and LPS-infused rats. In mesenteric arteries, LPS treatment suppressed the potentiation of the neurogenic responses by the alpha2-adrenoceptor antagonist, yohimbine and by the inhibitor of neuronal uptake of noradrenaline, cocaine. In rat tail artery exposed to L-arginine, LPS treatment produced an increase in [3H]-noradrenaline overflow evoked by electrical stimulation. Altogether, these data suggest that an enhanced noradrenaline release from sympathetic nerves, probably resulting from inhibition of the modulatory effect of both prejunctional alpha2-adrenoceptors and neuronal uptake mechanism, may play a role in the preservation of neurogenic response after LPS treatment despite evidence of the induction of NO synthase.
authors.affiliation: Pharmacologie et physico-chimie des interactions cellulaires et moléculaires, UMR CNRS 7034, Faculté de pharmacie, Université Louis Pasteur, Illkirch, France.
authors.forename: P
authors.initials: P
authors.lastname: Ohlmann
authors.forename: M C
authors.initials: MC
authors.lastname: Martínez
authors.forename: B
authors.initials: B
authors.lastname: Bucher
authors.forename: R
authors.initials: R
authors.lastname: Andriantsitohaina
authors.forename: B
authors.initials: B
authors.lastname: Muller
authors.forename: F
authors.initials: F
authors.lastname: Schneider
authors.forename: J C
authors.initials: JC
authors.lastname: Stoclet
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D001158:Arteries / Q000294:innervation / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D003042:Cocaine / Q000494:pharmacology; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004926:Escherichia coli; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008638:Mesenteric Arteries / Q000294:innervation* / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000378:metabolism*; D013623:Tail / Q000098:blood supply*; D014661:Vasoconstriction / Q000187:drug effects; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D015016:Yohimbine; D009569:Nitric Oxide; D001120:Arginine; D003042:Cocaine; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine