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Role of B1 adrenergic receptor in cardiac responsiveness during thyrotoxicosis

Alterations in cardiac functions are observed in patients with thyrotoxicosis, similar to those observed in state of hyper‐stimulation of the Sympathetic Nervous System. Nonetheless, the circulating levels of catecholamine are normal, suggesting that the T3 increases adrenergic responsiveness in the heart. To evaluate this hypothesis, we studied mice with knockout for B1 adrenergic receptor (KOB1), the main isoform in the heart submitted thyrotoxicosis by treatment with T3 (20ng/g BW) for 21 days. Our data indicates that the increase in the heart rate induced by T3 was similar in wild type and KOB1 mice (637±33.7 bpm and 630±44.5 bpm, respectively) but significantly higher when compared to not treated wild type and KOB1(573±35 and 514±18, respectively). Similar results were found for systolic blood pressure and diastolic blood pressure. However, wild type mice increased their left ventricular weight in response to T3 (5±1.2 vs. ctrl 3.5±0.18 mg/BW), but not KOB1(5.1±0.96 vs. ctrl 4.5±1.05 mg/BW). Our results suggest that the cardiac alterations during thyrotoxicosis are due to a direct effect of T3 in the heart and do not seem to depend on adrenergic signaling mediated by B1 adrenergic receptor.