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Does amiodarone affect heart rate by inhibiting the intracellular generation of triiodothyronine from thyroxine?

1984; Wiley; Volume: 82; Issue: 1 Linguagem: Inglês

10.1111/j.1476-5381.1984.tb16468.x

1476-5381

Maja T. Lindenmeyer, Stefan Spörri, M Stäubli, A. Studer, H Studer,

Cardiac electrophysiology and arrhythmias

The hypothesis that the antiarrhythmic drug amiodarone slows down the heart rate by its inhibitory action on the intracellular conversion of thyroxine (T 4 ) to 3,5,3′ triiodothyronine (T 3 ) was investigated. For this purpose we compared the effect of amiodarone with that of another potent inhibitor of the T 4 → T 3 conversion, i.e. the radiographic contrast medium iopanoic acid, on the heart rate of unanaesthetized guinea‐pigs. Both amiodarone and, to an even greater extent, iopanoic acid induced an increase in serum 3.5′,3′ triiodothyronine (reverse T 3 ), indicating effective inhibition of T 4 → T 3 conversion. Both amiodarone and iopanoic acid were accumulated in the liver and in the heart (measured as iodine). While amiodarone induced bradycardia, iopanoic acid did not change the heart rate. Supraphysiological amounts of exogenous T 3 reverted the amiodarone induced bradycardia to near normal values. A comparable effect was observed with isoprenaline. The intracellular inhibition of the T 4 → T 3 conversion is not the ultimate mode of the action of the amiodarone effect on heart rate. It is thought that amiodarone interacts with T 3 at its receptor or somewhere later along the pathway from the T 3 ‐receptor interaction to the final effect of T 3 on heart rate.