| http://purl.uniprot.org/citations/15838359 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15838359 | http://www.w3.org/2000/01/rdf-schema#comment | "Endothelin-1 (ET-1) is involved in the pathogenesis of cardiac and renal hemodynamic changes and impaired excretory function in congestive heart failure. It has previously been demonstrated that acute administration of ABT-627 (endothelin-A blocker) abolished systemic and renal vasoconstriction in controls and rats with congestive heart failure induced by a surgically created aortocaval fistula (Abassi et al. Clin Sci (Lond) 2002;103:S245-S248). In contrast, acute endothelin-B blockade by A-192621 exaggerated the ET-1 induced systemic and renal vasoconstriction. The present study examined the renal and systemic effects of chronically administered ABT-627 (24 mg/kg per day) or A-192621 (72 mg/kg per day) for 7 days via osmotic minipumps inserted intraperitoneally on the day of operation of sham controls and rats with congestive heart failure. Tailcuff measurements revealed that ABT-627 significantly decreased mean arterial pressure from 108 +/- 2 mmHg to 87 +/-2 mmHg (P < 0.05), whereas A-192621 significantly increased mean arterial pressure from 110 +/- 3 mmHg to 122 +/-3 mmHg (P < 0.05) in controls. Despite the hypotensive effect of ABT-627, daily sodium excretion dramatically increased, but to a lesser extent in A-192621-treated controls. Furthermore, chronic administration of ABT-627 to controls attenuated the systemic and renal vasoconstriction induced by ET-1 (1 nmol/kg intravenous), whereas A-192621 augmented these effects. Similarly, chronic treatment with ABT-627 totally abolished the systemic and renal vasoconstriction caused by injected ET-1 in rats with congestive heart failure, whereas A192621 potentiated these effects. Chronic treatment of animals with congestive heart failure with ABT-627 did not influence daily sodium excretion, whereas treatment with A192621 significantly improved daily sodium excretion. Interestingly, treatment with either ABT-627 or A192621 significantly decreased cardiac hypertrophy in rats with congestive heart failure. In conclusion, in sham controls endothelin-B receptor mediated vasodilation and natriuresis, probably as a result of tubular action, whereas in congestive heart failure the excretory contribution of endothelin-B receptor was attenuated, resulting in Na+ retention."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.org/dc/terms/identifier | "doi:10.1097/01.fjc.0000166214.42791.f2"xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/author | "Hoffman A."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/author | "Abassi Z."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/author | "Francis B."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/author | "Winaver J."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/author | "Karram T."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/name | "J Cardiovasc Pharmacol 44 Suppl"xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/pages | "S54-8"xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/title | "Renal and systemic effects of chronic blockade of ET(A) or ET(B) receptors in normal rats and animals with experimental heart failure."xsd:string |
| http://purl.uniprot.org/citations/15838359 | http://purl.uniprot.org/core/volume | "1"xsd:string |
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