PT - JOURNAL ARTICLE AU - OSAMU HAZEKI AU - MICHIO UI TI - <em>Beta</em><sub>1</sub>- and <em>Beta</em><sub>2</sub>-Adrenergic Receptors Responsible for Cyclic AMP Accumulation in Isolated Heart and Lung Cells DP - 1980 Jan 01 TA - Molecular Pharmacology PG - 8--13 VI - 17 IP - 1 4099 - http://molpharm.aspetjournals.org/content/17/1/8.short 4100 - http://molpharm.aspetjournals.org/content/17/1/8.full SO - Mol Pharmacol1980 Jan 01; 17 AB - Cells isolated from adult rat heart and lung by the collagenase method were incubated with the addition of general or selective beta-adrenergic agonists and antagonists and were analyzed for changes in the cyclic AMP content as an index of the cellular adenylate cyclase activity. On the basis of concentrations required for half-maximal increase in the cyclic AMP content, norepinephrine was as potent in heart cells as, but much less potent in lung cells than, epinephrine. Practolol, a selective beta1 antagonist, was more potent in heart cells than in lung cells, whereas butoxamine, a selective beta2 antagonist, was more potent in lung cells than in heart cells. Thus, adenylate cyclase-linked beta-adrenergic receptors were characterized as beta1 in heart cells and as beta2 in lung cells. All of the beta2 agonists tested, salbutamol, trimetoquinol and procaterol, showed much lower intrinsic activities than epinephrine, norepinephrine or isoproterenol in increasing cyclic AMP contents in heart cells, indicating that the intrinsic activity observed in heart cells may serve as an additional criterion for classification of beta1 and beta2 agonists. Concentrations of adrenergic agonists required for the half-maximal increase in cyclic AMP, as well as concentrations of adrenergic antagonists required for the half-maximal decrease of the epinephrine-induced accumulation of the nucleotide, in heart and lung cells were well correlated with the dissociation constants for their specific binding to membrane preparations of the same tissues. Thus, measurement of cyclic AMP in isolated heart and lung cells may provide a simple and convenient assay system for screening new, potentially specific, beta-adrenergic agonists and antagonists.