Abstract
Hyperthyroidism is associated with elevation of heart cells sensitivity to catecholamines. We demonstrated that T 3(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 T 3-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 ( K d ). 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.
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