rdf:type |
|
lifeskim:mentions |
umls-concept:C0022646,
umls-concept:C0030685,
umls-concept:C0033567,
umls-concept:C0034493,
umls-concept:C0042396,
umls-concept:C0079281,
umls-concept:C0079284,
umls-concept:C0205263,
umls-concept:C0391871,
umls-concept:C0597357,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1414262,
umls-concept:C1549542,
umls-concept:C1720127,
umls-concept:C1879547,
umls-concept:C1963578,
umls-concept:C2348358
|
pubmed:issue |
2-3
|
pubmed:dateCreated |
1993-10-4
|
pubmed:abstractText |
Endothelin-1 (0.005 and 0.01 nmol) induced a dose-dependent increase in perfusion pressure in the perfused rabbit kidney. These pressor effects were markedly reduced by an endothelin ETA receptor antagonist, BQ-123 (0.1 microM). Similarly, the release of prostacyclin triggered by intra-arterial infusion of endothelin-1 (10 nM) was significantly reduced in a concentration-dependent manner when the kidney was pretreated with BQ-123 (0.5-1 microM). In contrast, two selective ETB receptor agonists, BQ-3020 and IRL 1620, were found to be inactive, both as pressor agents and releasers of prostacyclin at doses (for the pressor effects) and concentrations (for the prostacyclin generation) 50-100 times higher than those of endothelin-1. BQ-123 (1 microM) did not modify the pressor or prostanoid-releasing properties of angiotensin II. These results confirm our previous observations suggesting that pressor responses and prostanoid release induced by endothelin-1 are mediated via the selective activation of ETA receptors in the perfused rabbit kidney.
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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/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/BQ 3020,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins,
http://linkedlifedata.com/resource/pubmed/chemical/Epoprostenol,
http://linkedlifedata.com/resource/pubmed/chemical/IRL 1620,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Endothelin A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin,
http://linkedlifedata.com/resource/pubmed/chemical/cyclo(Trp-Asp-Pro-Val-Leu)
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0014-2999
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
24
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pubmed:volume |
237
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
275-81
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8365455-Angiotensin II,
pubmed-meshheading:8365455-Animals,
pubmed-meshheading:8365455-Dose-Response Relationship, Drug,
pubmed-meshheading:8365455-Endothelins,
pubmed-meshheading:8365455-Epoprostenol,
pubmed-meshheading:8365455-Female,
pubmed-meshheading:8365455-Kidney,
pubmed-meshheading:8365455-Male,
pubmed-meshheading:8365455-Peptide Fragments,
pubmed-meshheading:8365455-Peptides, Cyclic,
pubmed-meshheading:8365455-Perfusion,
pubmed-meshheading:8365455-Rabbits,
pubmed-meshheading:8365455-Receptor, Endothelin A,
pubmed-meshheading:8365455-Receptors, Endothelin,
pubmed-meshheading:8365455-Vasoconstriction
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pubmed:year |
1993
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pubmed:articleTitle |
Endothelin-1 induces vasoconstriction and prostacyclin release via the activation of endothelin ETA receptors in the perfused rabbit kidney.
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pubmed:affiliation |
Department of Pharmacology, Medical School, Université de Sherbrooke, Canada.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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