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The metabolic and cardiovascular effects of hyperthyroidism are largely independent of β-adrenergic stimulation

Endocrinology, ISSN: 0013-7227, Vol: 145, Issue: 6, Page: 2767-2774
2004
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Article Description

Hyperthyroidism and states of adrenergic hyperactivity have many common clinical features, suggesting similar pathogenic mechanisms of action. The widespread use of β-adrenergic receptor (βAR) antagonists (β-blockers) to treat hyperthyroidism has led to the belief that the physiological consequences of thyroid hormone (TH) excess are mediated in part via catecholamine signaling through βARs. To test this hypothesis, we compared the response to TH excess in mice lacking the three known βARs (β-less) vs. wild-type (WT) mice. Although β-less mice had a lower heart rate at baseline in comparison to WT mice, the metabolic and cardiovascular responses to hyperthyroidism were equivalent in both WT and β-less mice. These data indicate that the metabolic and cardiovascular effects of TH excess are largely independent of βARs. These findings suggest that the efficacy of clinical treatment of hyperthyroidism with β-blockers is due to antagonism of sympathetic signaling, and that this process functions independently of TH action.

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