Administration of apomorphine to rats leads to a temporary decrease in adrenal catecholamines and a long-term increase in adrenal tyrosine hydroxylase activity. The kinetic characteristics of tyrosine hydroxylase of the apomorphine-treated and control rats were determined. A significant increase in V max was observed in the treated group as compared to controls; however, there was no change in the K m for the cofactor DMPH 4 or tyrosine between the two groups in undialyzed or dialyzed preparations, indicating that the increase in tyrosine hydroxylase activity was probably due to an increase in enzyme protein. The temporary decrease in adrenal catecholamines was found to be due to increased secretion after apomorphine treatment, even though the concentration of injected apomorphine appeared to be sufficient to inhibit adrenal tyrosine hydroxylase. This was further substantiated by the fact that the decrease in adrenal catecholamines was prevented by adrenal denervation. The delayed increase in tyrosine hydroxylase activity after apomorphine treatment was observed in hypophysectomized rats; however, it was abolished after splanchnic nerve transection. A relationship was sought between the decrease in adrenal catecholamines and increase in adrenal tyrosine hydroxylase activity. When apomorphine and L-3,4-dihydroxyphenylalanine ( L-DOPA) were administered simultaneously, there was no short-term decrease in adrenal catecholamine content but the increased tyrosine hydroxylase activity was still observed. Also, the administration of α-methyl- p-tyrosine to rats decreased the concentration of adrenal catecholamines and yet did not affect adrenal tyrosine hydroxylase activity. The results suggest that increased nerve activity, and not adrenal catecholamine concentrations, regulates the induction of adrenal tyrosine hydroxylase. Furthermore, regulation would be by way of some central mechanism involving dopamine-sensitive receptors.