SB 209670 inhibits the arrhythmogenic actions of endothelin-1 in the anesthetized dog.
J Cardiovasc Pharmacol
; 31 Suppl 1: S99-102, 1998.
Article
en En
| MEDLINE
| ID: mdl-9595411
ABSTRACT
SB 209670 reduced basal mean arterial pressure (16%) without affecting left-circumflex coronary artery (LCX) flow, cardiac output, heart rate, or global/regional myocardial contractility. In vehicle-treated animals, i.e. endothelin (ET)-1 produced an initial hyperemic response in the LCX, followed by a secondary reduction in flow. This response was accomplished by decreases in LCX regional wall fractional shortening, +dP/dt and -dP/dt, but an increase in left anterior wall fractional shortening. ET-1 also produced dose-related, fatal ventricular fibrillation. Whereas SB 209670 administration did not inhibit the initial increase in coronary flow produced by ET-1, the secondary constrictor responses were markedly antagonized. SB 209670 also attenuated the reduction in LCX regional wall fractional shortening and converted the increase in left anterior wall contractility to a reduction in contractility. Although SB 209670 produced only a modest inhibition of the ET-1-mediated reductions in dP/dt, the induction of fatal ventricular arrhythmias was completely abolished. Therefore, the data are consistent with the hypothesis that the coronary ischemic and proarrythmic actions of ET-1 are distinct. Therefore, ET receptor antagonists may be useful in treatment of disturbances in cardiac rhythm.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Arritmias Cardíacas
/
Endotelina-1
/
Antagonistas de los Receptores de Endotelina
/
Indanos
Límite:
Animals
Idioma:
En
Revista:
J Cardiovasc Pharmacol
Año:
1998
Tipo del documento:
Article
País de afiliación:
Estados Unidos