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  • Title: Amiodarone has exclusively non-genomic action on cardiac beta-adrenoceptor regulation.
    Author: Vassy R, Starzec A, Yin Y, Nicolas P, Perret GY.
    Journal: Eur J Pharmacol; 2000 Nov 24; 408(3):227-32. PubMed ID: 11090638.
    Abstract:
    The antiarrhythmic drug amiodarone down-regulates the density of cardiac beta-adrenoceptors behaving as a triiodothyronine (T(3)) antagonist. It is still unclear if amiodarone acts at the nuclear (genomic) and/or the non-genomic levels. Using Northern blot analysis, we showed that the amiodarone had no effect on the increase of beta(1)-adrenoceptor mRNA level induced by the T(3)-administration in the heart of thyroidectomised rats. Thus, our results suggest that amiodarone has no genomic effect. Consequently, we investigated whether amiodarone down-regulation of beta-adrenoceptor number in T(3)-stimulated cardiomyocytes could be explained by changes in the rate of cell surface receptor protein turnover. Indeed, the binding studies of cyclohexidemide-treated cells showed that amiodarone suppressed the T(3)-induced decrease in the rate of the cell surface receptor disappearance. In conclusion, our findings indicate that the modulation of cardiac beta-adrenoceptor density by amiodarone involves only non-genomic targets required in T(3)-dependent regulation of the cell surface beta-adrenoceptor turnover.
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