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Research Article Free access | 10.1172/JCI109288

The Influence of Hyperthyroidism and Hypothyroidism on the β-Adrenergic Responsiveness of the Turkey Erythrocyte

John P. Bilezikian, John N. Loeb, and Donald E. Gammon

Department of Medicine, College of Physicians and Surgeons, Columbia University, New York 10032

Find articles by Bilezikian, J. in: PubMed | Google Scholar

Department of Medicine, College of Physicians and Surgeons, Columbia University, New York 10032

Find articles by Loeb, J. in: PubMed | Google Scholar

Department of Medicine, College of Physicians and Surgeons, Columbia University, New York 10032

Find articles by Gammon, D. in: PubMed | Google Scholar

Published February 1, 1979 - More info

Published in Volume 63, Issue 2 on February 1, 1979
J Clin Invest. 1979;63(2):184–192. https://doi.org/10.1172/JCI109288.
© 1979 The American Society for Clinical Investigation
Published February 1, 1979 - Version history
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Abstract

The mechanisms responsible for altered adrenergic tone in hyperthyroidism and hypothyroidism are not fully understood. To investigate these mechanisms, the β-adrenergic receptor-cyclic AMP complex of the turkey erythrocyte was studied among groups of normal, hyperthyroid, and hypothyroid turkeys. In erythrocytes obtained from hypothyroid turkeys, there were fewer β-adrenergic receptors than in normal cells as determined by the specific binding of [125I]iodohydroxybenzylpindolol, as well as associated decreases both in catecholamine-responsive adenylate cyclase activity and in cellular cyclic AMP content. In contrast, erythrocytes obtained from hyperthyroid turkeys contained the same number of β-receptors and had the same catecholamine-responsive adenylate cyclase activity as cells from normal birds. Other characteristics of the β-receptors in cells from hyperthyroid birds were indistinguishable from those present in normal erythrocytes. However, within the range of circulating catecholamine concentrations, 5-50 nM, the erythrocytes of the hyperthyroid turkeys generated substantially more cyclic AMP after exposure to isoproterenol than did normal cells. These results suggest that thyroid hormone affects β-receptor-cyclic AMP interrelationships in the turkey erythrocyte by two distinct mechanisms: (a) In hypothyroidism, both β-receptors and catecholamine-dependent cyclic AMP formation are coordinately decreased; (b) in hyperthyroidism, β-receptors are unchanged but there is an amplification of the hormonal signal so that occupation of a given number of receptors at physiological concentrations of catecholamines leads to increased levels of cyclic AMP.

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