Abstract
MANY physiological responses of the cardiovascular system to thyroid hormone seem to reflect altered sympathetic activity. The effects of thyroid hormones on the heart are very similar to those induced by catecholamines and the possible interrelationship of these substances on myocardial function has been explained by an interaction at various levels. These include effects on altering catecholamine release from the sympathetic nervous system1,2, and modifying plasma catecholamine concentrations3,4, as well as tissue catecholamine content5 and responses6–8. Although several investigators have attempted to define an action of thyroid hormone and its possible role in potentiating the catecholamine response, the mechanism responsible for this modification has not been clarified. We have reported previously that physiological concentrations of L-triiodothyronine (T3) stimulate the rate of glucose metabolism in cultured heart cells prepared from newborn rats9. We now demonstrate here that cultured heart cells retain the characteristic of response to β-adrenergic stimulation and that this response seems to be influenced by T3.
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TSAI, J., CHEN, A. Effect of L-triiodothyronine on (−)3H-dihydroalprenolol binding and cyclic AMP response to (−)adrenaline in cultured heart cells. Nature 275, 138–140 (1978). https://doi.org/10.1038/275138a0
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DOI: https://doi.org/10.1038/275138a0
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