Hyperthyroidism is associated with elevation of heart cells sensitivity to catecholamines. We demonstrated that T3(10-8M) increased (30%) the number of β-adrenoceptors in intact heart cells grown in vitro within 48 hr, without changing the affinity of the ligand [3H]CGP-12177. The increase in β-adrenoceptors in T3-treated myocytes was not associated with an increase in receptor-mediated cAMP production. Amiodarone, an antiarrhythmic drug, reduces the sensitivity of the heart to catecholamines. To investigate this effect, we analysed the influence of amiodarone on the level of β-adrenergic receptors. Ninety minute preincubation with amiodarone (5 × 10-5 M) decreased the number of β-adrenoceptors (35-50%) in intact heart cells and in heart membranes, without affecting the dissociation constants (Kd). Amiodarone inhibited isoproterenol induced cAMP production. These results indicate that the mechanism of action of amiodarone on the heart seems to be a non-competitive inhibition of catecholamine receptors.