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Effects of prolonged noradrenaline infusion on the density of cardiac beta-adrenoceptors, phosphodiesterase (PDE) and adenylate cyclase (AC) activities, and the ability of NKH477, 6-(3-dimethylaminopropionyl) forskolin hydrochloride, to increase tension development and heart rate were studied in rat cardiac preparations. Noradrenaline infusion (400 micrograms/kg/hr, s.c.) for 7 days significantly decreased cardiac beta-adrenoceptor density (Bmax), whereas the binding affinity (Kd) of the ligand was unchanged. The basal cardiac PDE activity was increased in treated rats, whereas there was no difference in the basal cardiac AC activity between treated and untreated rats. Significant decreases in basal developed tension and heart rate were observed in the left and right atrial muscles from treated rats, respectively. The positive inotropic and chronotropic potencies of NKH477 were unaffected by noradrenaline infusion, whereas the positive inotropic potencies of isoproterenol and 3-isobutyl-1-methylxanthine were significantly reduced. Thus, NKH477 appears to be superior to beta-adrenoceptor agnosits or PDE inhibitors as a cardiotonic drug in the treatment of heart failure accompanied by beta-adrenoceptor downregulation.

Effectiveness of NKH477, a novel forskolin derivative, in rat cardiac preparations with desensitized .BETA.-adrenoceptors.