The inhibitory action of hydralazine on the contractility of human blood vessels has been examined by using in vitro human digital artery and metacarpal vein preparations obtained postmortem. Cumulative contractile concentration-effect curves were performed to norepinephrine, 5-hydroxytryptamine, histamine, angiotensin, KCl and barium chloride (in both arteries and veins. With the exception of barium chloride, hydralazine shifted the concentration-effect curves to the right and reduced the maximum responses to these agonists. This effect was markedly greater in arteries than in veins in which hydralazine had no effect. The maximum responses to the agonists norepinephrine, 5-hydroxytryptamine and KCl were markedly reduced when the normal bathing solution was replaced by a calcium-free solution, and for each agonist this effect was much greater in veins than arteries. The responses to barium chloride, however, were not significantly altered by the calcium-free bathing solution. It is concluded that human arteries are much more sensitive to the effects of hydralazine than are human veins and that the mechanism of action of hydralazine is probably due to inhibition of the release of tightly bound calcium ions.