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Article: Cardiac and vascular effects of nitric oxide synthase inhibition in lipopolysaccharide-treated rats

TitleCardiac and vascular effects of nitric oxide synthase inhibition in lipopolysaccharide-treated rats
Authors
Keywordsβ-adrenergic stimulation
Ca2+ transient
Lipopolysaccharide
Nitric oxide (NO)
Vascular hyporeactivity
Ventricular myocyte
Issue Date2000
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2000, v. 406 n. 2, p. 257-264 How to Cite?
AbstractIn the present study, intraperitoneal injection of lipopolysaccharide (10 mg/kg) to anaesthetized rats produced a gradual fall in mean arterial pressure in 6 h. Aortic rings from lipopolysaccharide-treated rats showed a significant reduction in the contractile response to vasoconstrictors. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME) or aminoguanidine, two nitric oxide synthase (NOS) inhibitors, abolished this vascular hyporeactivity. In ventricular myocytes isolated from lipopolysaccharide-treated rats, both electrically induced Ca2+ transients and the intracellular Ca2+ response to β-adrenergic stimulation were significantly depressed when compared with those recorded from myocytes from sham control rats. L-NAME and aminoguanidine alone had no effects on electrically stimulated Ca2+ transients in ventricular myocytes either from control or lipopolysaccharide-treated rats. However, these two NOS inhibitors augmented the intracellular Ca2+ response to β-adrenergic stimulation in myocytes from lipopolysaccharide-treated rats, but not in control myocytes. In addition, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of nitric oxide (NO)-sensitive guanylyl cyclase, also reversed the intracellular Ca2+ hyporesponsiveness to β-adrenergic stimulation in myocytes from lipopolysaccharide-treated rats. In cardiac myocytes from lipopolysaccharide-rats pretreated with aminoguanidine, the intracellular Ca2+ hyporesponsiveness to β-adrenergic stimulation was abolished. However, there still existed a depressed Ca2+ response to electrical field stimulation. These data indicate that NO following lipopolysaccharide stimulation contributes to vascular hyporeactivity and the depressed intracellular Ca2+ response to β-adrenergic stimulation in lipopolysaccharide-treated rats, but is not responsible for the reduced Ca2+ response to electrical stimulation in our experimental conditions. (C) 2000 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/81219
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShan, Qen_HK
dc.contributor.authorBourreau, JPen_HK
dc.date.accessioned2010-09-06T08:15:10Z-
dc.date.available2010-09-06T08:15:10Z-
dc.date.issued2000en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2000, v. 406 n. 2, p. 257-264en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81219-
dc.description.abstractIn the present study, intraperitoneal injection of lipopolysaccharide (10 mg/kg) to anaesthetized rats produced a gradual fall in mean arterial pressure in 6 h. Aortic rings from lipopolysaccharide-treated rats showed a significant reduction in the contractile response to vasoconstrictors. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME) or aminoguanidine, two nitric oxide synthase (NOS) inhibitors, abolished this vascular hyporeactivity. In ventricular myocytes isolated from lipopolysaccharide-treated rats, both electrically induced Ca2+ transients and the intracellular Ca2+ response to β-adrenergic stimulation were significantly depressed when compared with those recorded from myocytes from sham control rats. L-NAME and aminoguanidine alone had no effects on electrically stimulated Ca2+ transients in ventricular myocytes either from control or lipopolysaccharide-treated rats. However, these two NOS inhibitors augmented the intracellular Ca2+ response to β-adrenergic stimulation in myocytes from lipopolysaccharide-treated rats, but not in control myocytes. In addition, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of nitric oxide (NO)-sensitive guanylyl cyclase, also reversed the intracellular Ca2+ hyporesponsiveness to β-adrenergic stimulation in myocytes from lipopolysaccharide-treated rats. In cardiac myocytes from lipopolysaccharide-rats pretreated with aminoguanidine, the intracellular Ca2+ hyporesponsiveness to β-adrenergic stimulation was abolished. However, there still existed a depressed Ca2+ response to electrical field stimulation. These data indicate that NO following lipopolysaccharide stimulation contributes to vascular hyporeactivity and the depressed intracellular Ca2+ response to β-adrenergic stimulation in lipopolysaccharide-treated rats, but is not responsible for the reduced Ca2+ response to electrical stimulation in our experimental conditions. (C) 2000 Elsevier Science B.V.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology. Copyright © Elsevier BV.en_HK
dc.subjectβ-adrenergic stimulationen_HK
dc.subjectCa2+ transienten_HK
dc.subjectLipopolysaccharideen_HK
dc.subjectNitric oxide (NO)en_HK
dc.subjectVascular hyporeactivityen_HK
dc.subjectVentricular myocyteen_HK
dc.titleCardiac and vascular effects of nitric oxide synthase inhibition in lipopolysaccharide-treated ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=406&issue=2&spage=257&epage=264&date=2000&atitle=Cardiac+and+vascular+effects+of+nitric+oxide+synthase+inhibition+in+lipopolysaccharide-treated+ratsen_HK
dc.identifier.emailBourreau, JP: bourreau@hkucc.hku.hken_HK
dc.identifier.authorityBourreau, JP=rp00389en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-2999(00)00660-9en_HK
dc.identifier.pmid11020489-
dc.identifier.scopuseid_2-s2.0-0034644866en_HK
dc.identifier.hkuros63622en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034644866&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume406en_HK
dc.identifier.issue2en_HK
dc.identifier.spage257en_HK
dc.identifier.epage264en_HK
dc.identifier.isiWOS:000089774400012-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridShan, Q=7007145043en_HK
dc.identifier.scopusauthoridBourreau, JP=7003927886en_HK

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