Although evidence is limited and derived from many studies with many different objectives on a variety of blood vessels under varying experimental conditions, it appears that the human adrenergic vascular neuroeffector mechanism is qualitatively similar to that defined in studies on animals. The characteristics of the alpha-adrenoceptor based upon pA2 measurements and other pharmacological characteristics show it to be similar to adrenoreceptors defined in animals. The sensitivity of vascular smooth muscle to norepinephrine is of the same order throughout the human vasculature and is similar to that seen in most animal vessels. In most blood vessels the alpha-adrenoreceptor is the dominant type. By contrast the beta-adrenoceptor component is usually small with a high threshold except in the coronary artery and facial vein. Sympathetic frequency-response relationships of both arteries and veins are similar to those from animal studies. The human alpha-adrenoceptor is coupled both to sequestered calcium sites and slow calcium channels, and these two mechanisms are responsible for the biphasic response of human blood vessels to norepinephrine. The slow calcium channel but not the sequestered calcium system is sensitive to calcium antagonists. There is evidence that the human adrenergic mechanism is altered in disease.