Experiments were designed to determine whether or not calcitonin, parathormone, and glucocorticoids have direct effects on the vascular smooth muscle cells of bone blood vessels. Tibias of mongrel dogs were isolated. The arteria nutriens was cannulated and perfused at constant flow with aerated Krebs-Ringer solution (37 degrees C). The perfusion pressure was continuously recorded. In unstimulated preparations calcitonin caused dose-dependent increases in perfusion pressure, indicating that it causes constriction of bone blood vessels. Parathormone did not affect basal perfusion; it did not significantly alter vasoconstrictions caused by the injection of norepinephrine indicating that the hormone has no direct effect on the vascular smooth muscle of bone blood vessels. Hydrocortisone, at low concentrations, augmented the constrictions caused by exogenous norepinephrine and periarterial nerve stimulation; at higher concentrations, hydrocortisone caused a dose-dependent inhibition of the response to adrenergic activation. The depressant effect of hydrocortisone was antagonized by propranolol, suggesting that the glucocorticoid facilitates beta-adrenergic relaxation of the vascular smooth muscle cells by catecholamines.