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Titolo:
CORONARY VASOCONSTRICTION BY ENDOTHELIN-1 IN ANESTHETIZED GOATS - ROLE OF ENDOTHELIN RECEPTORS, NITRIC-OXIDE AND PROSTANOIDS
Autore:
GARCIA JL; FERNANDEZ N; GARCIAVILLALON AL; MONGE L; GOMEZ B; DIEGUEZ G;
Indirizzi:
UNIV AUTONOMA MADRID,FAC MED,DEPT FISIOL,ARZOBISPO MORCILLO 2 E-28029MADRID SPAIN UNIV AUTONOMA MADRID,FAC MED,DEPT FISIOL E-28029 MADRID SPAIN
Titolo Testata:
European journal of pharmacology
fascicolo: 2, volume: 315, anno: 1996,
pagine: 179 - 186
SICI:
0014-2999(1996)315:2<179:CVBEIA>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARTERY; POTENT; RESPONSES; HETEROGENEITY; CONTRACTION; ANTAGONISTS; INHIBITION; ISCHEMIA; HEART;
Keywords:
CORONARY CIRCULATION; ENDOTHELIN ET(A) RECEPTOR; ENDOTHELIN ET(A) RECEPTOR; IRL 1620; BQ-123; NITRIC OXIDE (NO);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
J.L. Garcia et al., "CORONARY VASOCONSTRICTION BY ENDOTHELIN-1 IN ANESTHETIZED GOATS - ROLE OF ENDOTHELIN RECEPTORS, NITRIC-OXIDE AND PROSTANOIDS", European journal of pharmacology, 315(2), 1996, pp. 179-186

Abstract

The role of endothelin ET(A) and ET(B) receptors as well as of nitricoxide (NO) and prostanoids in the effects of endothelin-l on the coronary circulation was studied in anesthetized goats, where blood flow in the left circumflex coronary artery (coronary blood flow) (electromagnetically measured), systemic arterial pressure, left ventricle pressure and dP/dt, and heart rate were recorded. Endothelin-l (0.01-0.3 nmol), intracoronarily injected, produced marked, dose-dependent reductions in basal coronary blood flow, ranging from 5% for 0.01 nmol to 75%for 0.3 nmol; 0.1 and 0.3 nmol endothelin-l also reduced systolic ventricle pressure and dP/dt. The effects of endothelin-1 on coronary blood flow were diminished during intracoronary infusion of BQ-123 (cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp), specific antagonist for endothelin ET(A)receptors, 2-16 nmol/min) in a dose-dependent way, but not during theinfusion of BQ-788 yl]-1-(methoxycarbonyl)-D-tryptophyl]-D-norleucinemonosodium, specific antagonist for endothelin ET(B) receptors, 2-4 nmol/min). IRL 1620 (Suc-[Glu(9), Ala(11,15)]endothelin-1-(8-21), specific agonist for endothelin ET(B) receptors, 0.01-0.3 nmol), intracoronarily injected, slightly reduced basal coronary blood flow only when 0.1 and 0.3 nmol were applied (maximal reduction about 25%); 0.3 nmol IRL 1620 also reduced systolic ventricle pressure and dP/dt. The effects of IRL 1620 were not modified by BQ-123 or BQ-788. N-G-nitro-L-arginine methyl ester (L-NAME, inhibitor of NO synthesis, 47 mg/kg by i.v. route) reduced resting coronary blood flow by 10% and increased mean systemic arterial pressure and systolic ventricle pressure by 22 and 20%, respectively, without changing systolic ventricle dP/dt and heart rate. With L-NAME, the reductions of coronary blood flow by endothelin-l were potentiated (P < 0.05), and those by IRL 1620 were not changed (P > 0.05). Meclofenamate (cyclooxygenase inhibitor, 4-6 mg/kg by i.v.route) modified neither the basal values of hemodynamic variables northe coronary effects of endothelin-l and IRL 1620. Therefore, endothelin-l produces marked coronary vasoconstriction, which may be mediatedby endothelin ET(A) receptors, with no participation of endothelin ET(B) receptors. NO, but not prostanoids, may produce a basal coronary vasodilator tone and may inhibit endothelin-l-induced coronary vasoconstriction. Also, it is suggested that the coronary vasoconstriction by endothelin-l may impair cardiac performance due to heart ischemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:21:27