Molsidomine is an established drug for the treatment of coronary heart disease. It acts via the metabolite SIN-1 through liberation of NO. Experiments have proven the identity of NO and EDRF. Investigation of the molecular mechanism of action of molsidomine/SIN-1 indicate that molecular oxygen initiates NO formation through a one-electron abstraction from the intermediate. Ex vivo experiments in rats and in vitro studies in human coronary arteries showed that marked tolerance is induced with glyceryl trinitrate, whereas prolonged exposure to SIN-1 does not cause tolerance. Responsiveness to SIN-1 is not modified in nitrate-tolerant human arteries. Stimulation of soluble guanylate cyclase underlies the antiaggregatory actions of EDRF. Likewise SIN-1 inhibits platelet aggregation in various models. In dogs and pigs with critical stenosis molsidomine reduced significantly the frequency and the severity of cyclical reductions of coronary blood flow.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Vasodilatadores
/
Molsidomina
/
Inhibidores de Agregación Plaquetaria
/
Agregación Plaquetaria
/
Enfermedad Coronaria
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Blood Vessels
Año:
1990
Tipo del documento:
Article
Pais de publicación:
Suiza