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Article: Hyporesponsiveness to Ca 2+ of aortic smooth muscle in endotoxin- treated rats: No-dependent and -independent in vitro mechanisms

TitleHyporesponsiveness to Ca 2+ of aortic smooth muscle in endotoxin- treated rats: No-dependent and -independent in vitro mechanisms
Authors
Issue Date1996
Citation
Research Communications In Molecular Pathology And Pharmacology, 1996, v. 92 n. 3, p. 275-284 How to Cite?
AbstractThe aim of this study was to assess the nature of vascular hyporeactivity to vasopressor agents in rats with endotoxemia. Endotoxemia was induced in rats by bacterial endotoxin (E. Coli lipopolysaccaharide, LPS). In LPS-treated rats, the reactivity of endothelium-denuded aortic rings to phenylephrine (PE) and potassium chloride (KCl) was characterized by a decreased magnitude of contraction, a slower onset of contraction and a faster rate of relaxation when compared to the control aortic rings. Addition of L-arginine (L-arg), the substrate of nitric oxide synthase (NOS), but not D-arginine (D-arg), reduced further PE-induced contraction in rings from LPS- treated rats. Inhibition of contraction in rings of LPS-treated rats was partially antagonized by the inhibitor of NOS, N(ω)-nitro-L-arginine methyl ester (L-NAME). Thus, production of non-endothelial nitric oxide (NO) was in part responsible for the hyporesponsiveness to PE. Rings from LPS-treated rats also displayed hyporeactivity and decreased sensitivity to Ca 2+ in depolarizing medium (60 mM K +). Hyporeactivity and hyposensitivity to Ca 2+ could only be partially reversed by L-NAME. The inhibitory effects of LPS- treatment on both PE- and KCl-induced aortic responses and the reversal effects of L-NAME confirm the contention that NO formation is involved in vascular hyporesponsiveness in endotoxic shock. The partial reversal by L- NAME of the hyporesponsiveness to KCl- and PE-induced contraction, and hyposensitivity to Ca 2+ in depolarized aorta suggest that factors other than the action of nonendothelial source of NO formation in vitro from L-arg also contribute to endotoxin-induced vascular hyporesponsiveness to vasopressor agents.
Persistent Identifierhttp://hdl.handle.net/10722/171625
ISSN
2002 Impact Factor: 0.315
2012 SCImago Journal Rankings: 0.107
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHo, KHen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:02Z-
dc.date.available2012-10-30T06:16:02Z-
dc.date.issued1996en_US
dc.identifier.citationResearch Communications In Molecular Pathology And Pharmacology, 1996, v. 92 n. 3, p. 275-284en_US
dc.identifier.issn1078-0297en_US
dc.identifier.urihttp://hdl.handle.net/10722/171625-
dc.description.abstractThe aim of this study was to assess the nature of vascular hyporeactivity to vasopressor agents in rats with endotoxemia. Endotoxemia was induced in rats by bacterial endotoxin (E. Coli lipopolysaccaharide, LPS). In LPS-treated rats, the reactivity of endothelium-denuded aortic rings to phenylephrine (PE) and potassium chloride (KCl) was characterized by a decreased magnitude of contraction, a slower onset of contraction and a faster rate of relaxation when compared to the control aortic rings. Addition of L-arginine (L-arg), the substrate of nitric oxide synthase (NOS), but not D-arginine (D-arg), reduced further PE-induced contraction in rings from LPS- treated rats. Inhibition of contraction in rings of LPS-treated rats was partially antagonized by the inhibitor of NOS, N(ω)-nitro-L-arginine methyl ester (L-NAME). Thus, production of non-endothelial nitric oxide (NO) was in part responsible for the hyporesponsiveness to PE. Rings from LPS-treated rats also displayed hyporeactivity and decreased sensitivity to Ca 2+ in depolarizing medium (60 mM K +). Hyporeactivity and hyposensitivity to Ca 2+ could only be partially reversed by L-NAME. The inhibitory effects of LPS- treatment on both PE- and KCl-induced aortic responses and the reversal effects of L-NAME confirm the contention that NO formation is involved in vascular hyporesponsiveness in endotoxic shock. The partial reversal by L- NAME of the hyporesponsiveness to KCl- and PE-induced contraction, and hyposensitivity to Ca 2+ in depolarized aorta suggest that factors other than the action of nonendothelial source of NO formation in vitro from L-arg also contribute to endotoxin-induced vascular hyporesponsiveness to vasopressor agents.en_US
dc.languageengen_US
dc.relation.ispartofResearch Communications in Molecular Pathology and Pharmacologyen_US
dc.titleHyporesponsiveness to Ca 2+ of aortic smooth muscle in endotoxin- treated rats: No-dependent and -independent in vitro mechanismsen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8827826-
dc.identifier.scopuseid_2-s2.0-0029659043en_US
dc.identifier.volume92en_US
dc.identifier.issue3en_US
dc.identifier.spage275en_US
dc.identifier.epage284en_US
dc.identifier.isiWOS:A1996UX35900002-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHo, KH=55205630300en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US

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