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pubmed-article:9321831pubmed:abstractTextLipopolysaccharide (LPS) induces cardiac depression by activating nitric oxide pathways to increase guanosine 3',5'-cyclic monophosphate (cGMP), a second messenger of nitric oxide. Endothelin-1 (ET-1) may interact with nitric oxide pathways. We hypothesized that ET-1 modulates LPS-induced contractile depression in cardiac myocytes. Adult rabbit cardiac myocytes exposed to LPS (10 ng/ml) developed decreased cell shortening after 6 h, with an increase in cardiac cGMP levels [606 +/- 36 (SE) fmol/mg protein] compared with control myocytes (360 +/- 26 fmol/mg protein, P < 0.05). LPS effects were completely blocked by coincubation with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (1 mM). Coincubation with ET-1 (10 nM) attenuated the contractile depression and increase in cGMP with LPS (482 +/- 28 fmol/mg protein, P < 0.05 vs. LPS alone). ET-1 alone did not alter cGMP levels (350 +/- 30 fmol/mg protein). ET-1 effects on contractile function were blocked by BQ-123 (10 microM), a selective ET-1 type A receptor antagonist. We conclude that ET-1 ameliorates LPS-induced contractile depression in cardiac myocytes by attenuating LPS effects on nitric oxide-cGMP pathways.lld:pubmed
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pubmed-article:9321831pubmed:authorpubmed-author:LeeW KWKlld:pubmed
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pubmed-article:9321831pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:9321831pubmed:year1997lld:pubmed
pubmed-article:9321831pubmed:articleTitleEndothelin-1 ameliorates contractile depression by lipopolysaccharide in cardiac myocytes.lld:pubmed
pubmed-article:9321831pubmed:affiliationDepartment of Medicine, Veterans Affairs San Diego Healthcare System, California, USA.lld:pubmed
pubmed-article:9321831pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9321831pubmed:publicationTypeResearch Support, U.S. Gov't, Non-P.H.S.lld:pubmed
pubmed-article:9321831pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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