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Titolo:
EFFECTS OF CALCIUM-ANTAGONISTS ON ENDOTHELIN-1-INDUCED MYOCARDIAL-ISCHEMIA AND EDEMA IN THE RAT
Autore:
FILEP JG; SKROBIK Y; FOURNIER A; FOLDESFILEP E;
Indirizzi:
UNIV MONTREAL,MAISONNEUVE ROSEMONT HOSP,RES CTR MONTREAL PQ H1T 2M4 CANADA INST NATL RECH SCI SANTE POINTE CLAIRE PQ H9R 1G6 CANADA
Titolo Testata:
British Journal of Pharmacology
fascicolo: 4, volume: 118, anno: 1996,
pagine: 893 - 900
SICI:
0007-1188(1996)118:4<893:EOCOEM>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; ENDOTHELIAL-CELLS; ISCHEMIA-REPERFUSION; CORONARY-ARTERY; RECEPTOR; PERMEABILITY; CHANNEL; VASOCONSTRICTION; VASODILATION; PROSTACYCLIN;
Keywords:
ENDOTHELIN; IRL 1620; ET(A) AND ET(B) RECEPTORS; CALCIUM; VERAPAMIL; NIFEDIPINE; MYOCARDIAL ISCHEMIA; VASCULAR PERMEABILITY; RAT HEART;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
J.G. Filep et al., "EFFECTS OF CALCIUM-ANTAGONISTS ON ENDOTHELIN-1-INDUCED MYOCARDIAL-ISCHEMIA AND EDEMA IN THE RAT", British Journal of Pharmacology, 118(4), 1996, pp. 893-900

Abstract

1 The effects of the calcium channel blockers, verapamil and nifedipine on myocardial ischaemia and oedema evoked by endothelin-1 (ET-1) orIRL 1620, an ET(B) receptor-selective agonist were studied in anaesthetized and conscious rats. 2 Bolus injection of ET-1 (1 nmol kg(-1), i.v.) or IRL 1620 (1 nmol kg(-1), i.v.) to conscious chronically catheterized rats evoked a transient depressor response followed by a prolonged presser effect. Corresponding to changes in blood pressure, a transient tachycardia and a sustained bradycardia were observed. Pretreatment of the animals with verapamil (1 mg kg(-1), i.v.) or nifedipine (200 mu g kg(-1), i.v.) produced on average 5 mmHg decrease in mean arterial blood pressure. Both verapamil and nifedipine inhibited by 63 and44% the presser actions of ET-1 or IRL 1620 (1 nmol kg(-1)), respectively, and the accompanying bradycardia. Both verapamil and nifedipine potentiated the magnitude of the depressor action of ET-1 and IRL 1620without affecting the accompanying tachycardia. Decreasing mean arterial blood pressure with hydralazine (0.2-0.3 mu mol kg(-1), i.v.) to levels comparable to those observed after verapamil or nifedipine had no significant effects on the haemodynamic responses to ET-1 or IRL-1620. 3 Intravenous bolus injection of ET-1 or IRL 1620 (0.1-2 nmol kg(-1)) into anaesthetized rats produced dose-dependent ST segment elevation of the electrocardiogram without causing arrhythmias. ST segment elevation developed within 30-50 s and persisted for at least 10-20 min following injection of the peptides.4 Pretreatment of the animals with verapamil (1 mg kg(-1), i.v.) or nifedipine (200 mu g kg(-1), i.v.) inhibited on average by 79 and 76% the ST segment elevation elicited by ET-1 (1 nmol kg(-1)), respectively. Verapamil and nifedipine also attenuated IRL 1620 (1 nmol kg(-1))-induced ST segment elevation on average by 71 and 74%, respectively. In contrast, no significant inhibition was observed with hydralazine (0.2-0.3 mu mol kg(-1)). 5 Both ET-1 and, to a lesser extent, IRL 1620 (0.1-2 nmol kg(-1)) evoked albumin accumulation in cardiac tissues in a dose-dependent fashion as measured bythe local extravascular accumulation of Evans blue dye in conscious rats. ET-1 and IRL 1620 (1 nmol kg(-1)) enhanced albumin extravasation by 109 and 82%, and 34 and 44% in the left ventricle and right atrium,respectively. ET-1 or IRL 1620-induced albumin extravasation was completely prevented by verapamil (1 mg kg(-1)) or nifedipine (200 mu g kg(-1)) in these vascular beds. In contrast, hydralazine (0.2-0.3 mu molkg(-1)) failed to modify the effects of ET-1 or IRL 1620 on albumin extravasation. 6 These results show that verapamil and nifedipine are highly effective in protecting the myocardium against the pro-ischaemicand microvascular permeability enhancing effects of ET-1 and suggest that ET(A) and constrictor ET(B) (tentatively termed ET(B2)) receptorsmediating these actions of ET-1 are coupled to calcium influx throughdihydropyridine-sensitive calcium channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 01:29:19