An overall review on prenylamine mechanisms of action in experimental models of myocardial damage.
In this review we present the effects of a well-known antianginal drug, prenylamine (PNL), in experimental models of acute myocardial damage induced by a beta-agonistic drug, isoproterenol (ISP), in several trials conducted in our laboratory in both rats (n = 204) and monkeys (n = 26). PNL significantly inhibited ISP-induced lesions, protecting the majority of animals studied. Studies dealing with the site of action of the drug, such as 45Ca, 3H-PNL and 3H-ISP trials, showed a clear membrane effect slowing down Ca transport. Correlation between ECG (inhibition of ST depression after ISP) and pathological findings in monkeys was also obtained in one of our experiments. These series of assays were useful in obtaining a more complete idea of activity and site of action of the drug. It seems that, in acute models, PNL acts as a calcium antagonistic drug rather than an adrenergic moderator.
D000787:Angina Pectoris / Q000188:drug therapy*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002428:Cebus; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects; D007545:Isoproterenol / Q000009:adverse effects; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011299:Prenylamine / Q000627:therapeutic use*; D051381:Rats; D011919:Rats, Inbred Strains; D012508:Sarcolemma / Q000187:drug effects
D007473:Ion Channels; D011299:Prenylamine; D007545:Isoproterenol; D002118:Calcium