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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Beta adrenoceptor interaction of full and partial agonists in the cat heart and soleus muscle.

The effects of a nonselective (isoproterenol), a beta-1 selective (prenalterol) and a beta-2-selective (procaterol) agonist on beta adrenoceptor occupancy, adenylate cyclase activity and muscle contractions in the myocardium (beta-1) and soleus muscle (beta-2) of the reserpine-pretreated cat were investigated. Each compound fully inhibited the specific binding of [125I] iodohydroxybenzylpindolol in both tissues. Myocardial and soleus muscle adenylate cyclase were equipotently activated by isoproterenol. Prenalterol and procaterol induced no more than marginal elevations in myocardial enzyme activity and only the latter compound produced an increase in soleus muscle adenylate cyclase activity (77% of that produced by isoproterenol). Prenalterol increased myocardial contractility (82% of that of isoproterenol) in a monophasic concentration-dependent manner, as did isoproterenol, whereas procaterol induced a biphasic inotropic response. The high affinity effect (23% of isoproterenol) of procaterol was selectively blocked by IPS 339 (beta-2-selective) and the low affinity component (70% of isoproterenol) was blocked by pamatolol (beta-1-selective). Isoproterenol and procaterol decreased subtetanic soleus muscle contractions equally, whereas prenalterol was devoid of effect in skeletal muscle. From the interrelations between the concentration-effect curves for these drug-induced responses, it was estimated that under the conditions used in these assays a full agonist in the heart has a spare beta-1 adrenoceptor pool of 80 to 90%. A corresponding beta-2 adrenoceptor reserve of 30 to 50% was derived from data obtained in the soleus muscle. On the basis of the present data, prenalterol may be characterized as a nonselective beta adrenoceptor ligand with beta-1 adrenoceptor partial agonistic activity.[1]


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