Bradykinin and related kinins are potent vasodilators. Inhibition of peripheral vascular smooth-muscle tone may result from actions of kinins at different levels. These include the afferent nociceptive nerve endings (bradykinin being a potent algesic agent); the brain and the spinal cord; and the three basic structural components of resistance vessels, namely, endothelium, smooth-muscle fibers, and autonomic nerve endings. The relative roles and the importance of these various structures and the mechanisms for the vasodilator and hypotensive effects of the kinins are discussed. Attention is focused on data obtained in isolated vascular beds, perfused with physiological media, and in strips or segments of arterial and venous vessels, suspended in vitro. Bradykinin and related kinins are potent vasodilators in the majority of peripheral vascular beds of various species, although they contract some isolated arteries and all the veins. These opposite vascular effects of the kinins appear to be mediated by at least two different receptor types, which have been identified and characterized with a series of kinin agonists and some kinin antagonists. B1-receptors mediate the contraction of arterial and venous smooth muscles, while B2-receptors are involved in the relaxation of arteries, the contraction of veins, and the increase in vascular permeability produced by kinins. Hypotension generally results from activation of B2-receptors, B1-receptors intervening only in special conditions. The relaxing effect of kinins in isolated arteries (B2-receptors) occurs only in the presence of endothelium, whereas all the stimulations do not require endothelium and appear to be owing to the activation of B2- and B1-receptors in the membranes of vascular smooth-muscle cells. It is still unknown whether endothelium is involved in the hypotensive and peripheral vasodilator actions of kinins in vivo.