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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1993-6-1
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pubmed:abstractText |
1. We have investigated whether local vascular production of nitric oxide or prostacyclin regulates venoconstriction induced by the endothelium-derived peptide, endothelin-1, in vivo in man. 2. Six healthy subjects received local dorsal hand vein infusion of endothelin-1 for 60 min alone or, on two separate occasions, co-infused with the donator of nitric oxide, glyceryl trinitrate, or the vasodilator prostaglandin, prostacyclin. In further studies, endothelin-1 was co-infused with an inhibitor of nitric oxide production, NG-monomethyl-L-arginine, or after oral administration of the irreversible inhibitor of prostaglandin production, acetylsalicylic acid (aspirin). 3. At a low dose (5 pmol/min), endothelin-1 alone caused slowly developing and long-lasting venoconstriction (maximal constriction: 66 +/- 4%). Although glyceryl trinitrate partially prevented endothelin-1-induced venoconstriction (maximum: 33 +/- 5%), inhibition of nitric oxide production did not affect endothelin-1-induced venoconstriction (maximum: 55 +/- 4%). 4. Prostacyclin was more effective at blocking the venoconstriction in response to endothelin-1 than glyceryl trinitrate (maximum: 12 +/- 3%), and there was substantial potentiation of endothelin-1-induced venoconstriction after pretreatment with aspirin (maximum: 90 +/- 3%). 5. Despite the capacity of nitric oxide to attenuate responses to endothelin-1, NG-monomethyl-L-arginine did not potentiate endothelin-1-induced venoconstriction, suggesting little or no stimulated production of nitric oxide in human veins. However, the potentiation of responses to endothelin-1 by aspirin indicates that endothelial production of prostacyclin attenuates responses to endothelin-1 in human veins in vivo.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Aspirin,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins,
http://linkedlifedata.com/resource/pubmed/chemical/Epoprostenol,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroglycerin,
http://linkedlifedata.com/resource/pubmed/chemical/omega-N-Methylarginine
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0143-5221
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
427-33
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8482047-Adult,
pubmed-meshheading:8482047-Arginine,
pubmed-meshheading:8482047-Aspirin,
pubmed-meshheading:8482047-Drug Synergism,
pubmed-meshheading:8482047-Endothelins,
pubmed-meshheading:8482047-Endothelium, Vascular,
pubmed-meshheading:8482047-Epoprostenol,
pubmed-meshheading:8482047-Humans,
pubmed-meshheading:8482047-Male,
pubmed-meshheading:8482047-Nitric Oxide,
pubmed-meshheading:8482047-Nitroglycerin,
pubmed-meshheading:8482047-Vasoconstriction,
pubmed-meshheading:8482047-omega-N-Methylarginine
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pubmed:year |
1993
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pubmed:articleTitle |
Endothelium-dependent modulation of responses to endothelin-I in human veins.
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pubmed:affiliation |
University of Edinburgh, Department of Medicine, Western General Hospital, U.K.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Comparative Study,
Randomized Controlled Trial,
Research Support, Non-U.S. Gov't
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