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Endocrinology, Vol 122, 2240-2246, Copyright © 1988 by Endocrine Society
ARTICLES |
J Segal
Charles A. Dana Research Institute, Boston, Massachusetts.
Thyroid hormone produces a prompt, plasma membrane-mediated increase in several metabolic functions in the rat thymocyte. These effects of thyroid hormone require calcium and are inhibited by the beta- adrenergic antagonist alprenolol. In the present study, the interrelationship between thyroid hormone and adrenergic agents, and the concept that calcium serves as the first messenger for the rapid action of thyroid hormone in the rat thymocyte are further examined. T3 produced a very rapid and dose-related increase in both 45 calcium accumulation and cytoplasmic free calcium concentration. These effects of T3, like its other calcium-dependent and prompt effects, were inhibited by beta-, but not by alpha-, adrenergic antagonists. Studies with selective beta-adrenergic agents revealed that the inhibitory effect was beta-1 in nature. In addition, beta-adrenergic agonists were found to promote additively T3 action, possibly through their beta-2 activity. Hence, the present study provides further support for the concept that calcium serves as the first messenger in the rapid, plasma membrane-mediated action of thyroid hormone in the rat thymocyte.
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