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- Title
Electrophysiological and haemodynamic effects of endothelin ETA and ETB receptors in normal and ischaemic working rabbit hearts.
- Authors
McCabe, Christopher; Hicks, Martin N.; Kane, Kathleen A.; Wainwright, Cherry L.
- Abstract
The aims of this study were to determine if endothelin-1 (ET-1) under normal and ischaemic conditions exhibits a direct arrhythmogenic effect that is independent of its ability to cause coronary vasoconstriction, and to determine the contribution of the ET(A) and ET(B) receptor subtype. ET(A/B) (with ET-1) and ET(A) (ET-1 in the presence of BQ-788) receptor activation resulted in a significant reduction in both epi- and endocardial monophasic action potential duration (MAPD(90)). ET(A) receptor activation reduced both epi- and endocardial effective refractory period (ERP). This MAPD(90) and ERP shortening were associated with a reduction in coronary flow, myocardial contractility and induction of ventricular fibrillation (VF) during ERP measurement. The ET(B) agonist sarafotoxin (S6c) had no marked, or concentration-dependent, effect on MAPD(90), ERP, myocardial contractility or induction of arrhythmias. Neither ET-1 nor S6c, given prior to coronary artery occlusion, significantly changed the ischaemia-induced dispersion of MAPD(90), ERP or the % incidence of VF. In conclusion, neither ET(A) nor ET(B) receptor stimulation has a direct arrhythmogenic effect in isolated rabbit hearts under normal or ischaemic conditions. The ET-1-induced arrhythmogenic effect observed in nonischaemic hearts is likely to be the result of the associated coronary vasoconstriction caused by ET(A) receptor stimulation resulting in myocardial ischaemia.
- Subjects
ENDOTHELINS; PEPTIDES; VASOCONSTRICTORS; HEART; CARDIOPULMONARY system; CARDIOVASCULAR system; RABBITS; PERICARDIUM physiology; ACTION potentials; ANIMAL experimentation; ARRHYTHMIA; BIOLOGICAL models; BLOOD pressure; CELL receptors; COMPARATIVE studies; CORONARY circulation; CORONARY disease; CARDIAC contraction; ENDOCARDIUM; RESEARCH methodology; MEDICAL cooperation; OLIGOPEPTIDES; PERICARDIUM; PIPERIDINE; SNAKE venom; RESEARCH; VENTRICULAR fibrillation; EVALUATION research; IN vitro studies; CHEMICAL inhibitors; PHARMACODYNAMICS; PHYSIOLOGY; CELL physiology
- Publication
British Journal of Pharmacology, 2005, Vol 146, Issue 1, p118
- ISSN
0007-1188
- Publication type
journal article
- DOI
10.1038/sj.bjp.0706304