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Titolo:
CHARACTERIZATION OF ENDOTHELIN-1-INDUCED VASCULAR EFFECTS IN THE RAT-HEART BY USING ENDOTHELIN RECEPTOR ANTAGONISTS
Autore:
WANG QD; LI XS; PERNOW J;
Indirizzi:
KAROLINSKA HOSP,DEPT CARDIOL S-17176 STOCKHOLM SWEDEN KAROLINSKA HOSP,DEPT CARDIOL S-17176 STOCKHOLM SWEDEN
Titolo Testata:
European journal of pharmacology
fascicolo: 1, volume: 271, anno: 1994,
pagine: 25 - 30
SICI:
0014-2999(1994)271:1<25:COEVEI>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; ETB-RECEPTOR; CORONARY FLOW; B RECEPTOR; POTENT; TONE; PROSTACYCLIN; CIRCULATION; IRL-1620; IRL-1038;
Keywords:
ENDOTHELIN RECEPTOR ANTAGONIST; CORONARY FLOW; ENDOTHELIN-1; ENDOTHELIN ET(A) RECEPTOR; ENDOTHELIN ET(B) RECEPTOR; NITRIC OXIDE (NO); VASOCONSTRICTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
Q.D. Wang et al., "CHARACTERIZATION OF ENDOTHELIN-1-INDUCED VASCULAR EFFECTS IN THE RAT-HEART BY USING ENDOTHELIN RECEPTOR ANTAGONISTS", European journal of pharmacology, 271(1), 1994, pp. 25-30

Abstract

The coronary vasoconstrictor effect of endothelin-1 was characterizedin the isolated rat heart by using the endothelin ET(A) receptor antagonist D-Asp-L-Pro-D-Val-L-Leu-D-Trp (BQ-123) and the endothelin ET(B)receptor antagonist [Cys(11)-Cys(15)]endothelin-1-(11-21) (IRL 1038). In addition, the involvement of nitric oxide and cyclooxygenase products was investigated. Endothelin-1 (0.012-0.4 nmol) dose dependently reduced coronary flow, which reached a maximum reduction of 83% at 0.4 nmol. BQ-123 (1 mu M) attenuated the responses to all doses of endothelin-1, whereas a lower concentration of BQ-123 (0.1 mu M) only reducedthe vasoconstriction due to the lower doses of endothelin-1 (0.012-0.12 nmol). In contrast, IRL 1038, which markedly antagonized the vasodilator response to the endothelin ET(B) receptor agonist Suc-[Glu(9),Ala(11,15)]endothelin-1-(8-21) (IRL 1620), significantly enhanced the endothelin-1-evoked coronary vasoconstriction. Endothelin-1 (0.04 nmol) reduced coronary flow by 61% in the presence of IRL 1038 as compared to 30% in the absence of the endothelin ET(B) receptor antagonist. The endothelin-1-evoked reduction in coronary flow was also significantly enhanced by the nitric oxide synthesis inhibitor N-G-nitro-L-arginine but was unaffected by the cyclooxygenase inhibitor diclofenac. IRL 1038 did not affect the response to endothelin-1 after blockade of nitricoxide synthesis. These results demonstrate that the coronary vasoconstriction induced by endothelin-1 in the isolated rat heart is a net effect of the stimulation of both endothelin ET(A) and endothelin ET(B) receptors. Thus, the endothelin ET(A) receptor mediates endothelin-1-evoked vasoconstriction whereas the endothelin ET(B) receptor stimulation counteracts the vasoconstriction by a mechanism depending on the release of nitric oxide.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/07/20 alle ore 05:49:14