title: The metabolic and cardiovascular effects of hyperthyroidism are largely independent of beta-adrenergic stimulation.
abstract: Hyperthyroidism and states of adrenergic hyperactivity have many common clinical features, suggesting similar pathogenic mechanisms of action. The widespread use of beta-adrenergic receptor (betaAR) antagonists (beta-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 betaARs. To test this hypothesis, we compared the response to TH excess in mice lacking the three known betaARs (beta-less) vs. wild-type (WT) mice. Although beta-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 beta-less mice. These data indicate that the metabolic and cardiovascular effects of TH excess are largely independent of betaARs. These findings suggest that the efficacy of clinical treatment of hyperthyroidism with beta-blockers is due to antagonism of sympathetic signaling, and that this process functions independently of TH action.
authors.affiliation: Beth Israel Deaconess Medical Center, Division of Endocrinology, Room 316, RN 99 Brookline Avenue, Boston, Massachusetts 02215, USA. ebachman@caregroup.harvard.edu
authors.forename: Eric S
authors.initials: ES
authors.lastname: Bachman
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Hampton
authors.forename: Harveen
authors.initials: H
authors.lastname: Dhillon
authors.forename: Ivo
authors.initials: I
authors.lastname: Amende
authors.forename: JuFeng
authors.initials: J
authors.lastname: Wang
authors.forename: James P
authors.initials: JP
authors.lastname: Morgan
authors.forename: Anthony N
authors.initials: AN
authors.lastname: Hollenberg
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D007545:Isoproterenol / Q000494:pharmacology; D051379:Mice; D011943:Receptors, Adrenergic, beta / Q000172:deficiency / Q000378:metabolism*; D014284:Triiodothyronine
chemical_list: D000318:Adrenergic beta-Agonists; D011943:Receptors, Adrenergic, beta; D014284:Triiodothyronine; D007545:Isoproterenol