Denopamine, which is an oral1y effective cardiotonic agent and a beta-1-receptor-selective agonist, reportedly prolongs the survival of the BIO 14.6 strain of cardiomyopathic Syrian hamsters(BIO). The latter is an animal model of human idiopathic cardiomyopathy. The purpose of the present experiment was to investigate the effects of denopamine on myocardial damage in BIO hamsters. They were divided into two groups: one that received denopamine treatment (1 mg/kg/day) from 2months of age, and a control (untreated) group. Morphological studies of the myocardium, assays for beta-adrenergic receptors, and measurements of myocardial adenylate cyclase (AC) activity and cAMP concentration were performed at 1,3, and 7months of age in al1 animals. It was observed that denopamine: 1) inhibited the progression of disease from the stage of hypertrophy to that of congestive failure that was demonstrated in the control BIO hamster, 2) inhibited the down-regulation of beta-1-adrenergic receptors in the myocardium of the control BIO hamsters at 7months of age, and 3) prevented an increase in myocardial AC activity and cAMP concentration that was seen in control BIO hamsters at 3months of age (stage of ealy hypertrophy). In conclusion, denopamine may prevent myocardial damage in BIO hamsters by inhibiting the down-regulation of beta-1-adrenergic receptors，thus preventing an increase in myocardial AC activity and cAMP concentration
