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
- 53Citations
- 36Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations53
- Citation Indexes53
- 53
- CrossRef32
- Captures36
- Readers36
- 36
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.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=2542476098&origin=inward; http://dx.doi.org/10.1210/en.2003-1670; http://www.ncbi.nlm.nih.gov/pubmed/15016719; https://academic.oup.com/endo/article/145/6/2767/2878271; https://dx.doi.org/10.1210/en.2003-1670; https://academic.oup.com/endo/article-abstract/145/6/2767/2878271?redirectedFrom=fulltext
The Endocrine Society
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