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The assumption that receptors in human blood cells reflect the status of receptors outside the circulation is supported by similar receptor numbers in animal and human tissues [4,8]. The increase in β-adrenergic receptors and the tendentiously higher activity of adenylate cyclase in thyrotoxic patients compared to euthyroid controls may represent a plausible mechanism for the reputed catecholamine supersensitivity in hyperthyroidism. Higher increases in β-adrenergic receptor numbers induced by short-term administration of exogenous thyroid hormones compared to long-term endogenous overproduction of thyroid hormones may be due to adaption of human cells to thyroid hormone excess. As in animals [4] it is suggested that the balance of α- and β-adrenergic receptors in humans is dependent on the thyroid state. The decrease in β-receptor numbers in the hypothyroid state may be associated with high catecholamine release in these patients. High variations in adrenergic receptor density suggest that adrenergic receptors are distinctly modulated in man. [ABSTRACT FROM AUTHOR]