The interactions of adrenergic agonists and thyroid hormones on the growth of erythroid colony-forming units were studied in cultures of dog marrow before and after the establishment of hypothyroidism. Erythroid colony growth in cultures from euthyroid dogs was enhanced by isoproterenol and other adrenergic agonists having β2-receptor specificity. With hypothyroidism, however, this responsiveness was lost, and sensitivity to α-agonists, such as phenylephrine and norepinephrine, was acquired. This alteration in receptor specificity appeared to be dependent upon thyroid hormone and was rapidly reversible. Preincubation of marrow cells from hypothyroid animals with thyroid hormone resulted in the reappearance of responsiveness to β-adrenergic agonists and the loss of sensitivity to α-agonists. These findings are in agreement with previous suggestions that β-adrenergic receptor activity is modulated by thyroid hormone levels and demonstrate that the specificity of adrenergic modulations of erythropoiesis in culture may accurately reflect the thyroid status of the intact animal.