Thyroid hormone regulation of rat heart, lymphocyte, and lung beta-adrenergic receptors.

In the rat, exogenous hyperthyroidism is associated with increased myocardial beta-adrenergic receptors. In man, however, despite the hyperadrenergic manifestations of thyrotoxicosis, lymphocyte beta-adrenergic receptors are unaltered. To test the hypothesis that lymphocytes do not reflect changes in myocardial beta-adrenergic receptors with hyperthyroidism, we characterized and quantified lymphocyte, myocardial, and lung (as another marker tissue) beta-adrenergic receptors in T3-treated rats. In T3-treated rats (500 microgram T3/kg.day for 3 days), myocardial beta-adrenergic receptors, as measured by [3H]dihydroalprenolol binding, increased by 60% over controls. In contrast, lymphocyte and lung beta-adrenergic receptors were unaltered. However, while lymphocyte adenylate cyclase activity was also unaltered with T3 treatment, lung adenylate cyclase activity was increased. Our data demonstrate that in rats, as in humans, hyperthyroidism is not associated with an increase in lymphocyte beta-adrenergic receptors. The differences in lymphocyte and myocardial receptors and lymphocyte and lung adenylate cyclases suggest that the response to T3 is a tissue-specific phenomenon. The data also suggest that despite the lack of increase in lymphocyte beta-adrenergic receptors in human hyperthyroidism, myocardial beta-adrenergic receptors may be increased.