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The Metabolic and Cardiovascular Effects of Hyperthyroidism Are Largely Independent of ß-Adrenergic Stimulation

Department of Medicine (E.S.B., H.D., A.N.H.), Division of Endocrinology; and Department of Medicine (T.G.H., I.A., J.W., J.P.M.), Division of Cardiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Eric S. Bachman, Beth Israel Deaconess Medical Center, Division of Endocrinology, Room 316, RN 99 Brookline Avenue, Boston, Massachusetts 02215. E-mail: ebachman{at}caregroup.harvard.edu.

Hyperthyroidism and states of adrenergic hyperactivity have many common clinical features, suggesting similar pathogenic mechanisms of action. The widespread use of ß-adrenergic receptor (ßAR) antagonists (ß-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 ßARs. To test this hypothesis, we compared the response to TH excess in mice lacking the three known ßARs (ß-less) vs. wild-type (WT) mice. Although ß-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 ß-less mice. These data indicate that the metabolic and cardiovascular effects of TH excess are largely independent of ßARs. These findings suggest that the efficacy of clinical treatment of hyperthyroidism with ß-blockers is due to antagonism of sympathetic signaling, and that this process functions independently of TH action.

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