A variety of physiological, pharmacological, and experimental factors are needed to explain why different authors have recorded often confusing and contradictory results of studying blood pressure and blood flow with vasopressin, oxytocin, and their analogs. Vasopressin and a number of synthetic analogs can produce potent constriction of numerous regional arteries and arterioles (e.g., splanchnic, renal, skeletal muscle, carotid, hepatic) in near physiological (i.e., 10(-12) - 10(-10)M) concentrations. Oxytocin appears to be able to elicit much weaker constriction (threshold = 10(-7) - 10(-5)M) and can produce relaxation (i.e., vasodilatation) in the presence of high degrees of tone in skeletal muscle, hepatic, renal, and splanchnic vasculatures; this may account for its blood pressure-lowering actions. With respect to the cerebral, coronary, and pulmonary vasculatures, there appears to be no good direct evidence indicating that either vasopressin or oxytocin can elicit much in the way of constrictor actions. Oxytocin, in contrast to vasopressin, is a potent constrictor of the umbilical-placental vasculature in concentrations found at term pregnancy and during parturition. Blood vessels from animals genetically lacking vasopressin appear to be supersensitive to the contractile actions of neurohypophyseal hormones. The contractile potencies and structure-activity relationships of neurohypophyseal peptides appears to vary with the type of blood vessel; i.v. rat pressor assays do not reflect the latter and cannot be utilized to determine structure-activity relationships of these peptides on vascular smooth muscle. Either a heterogeneity of the vasopressin receptor exists in peripheral blood vessels or there are vasopressin receptor subtypes on vascular muscles. Oxytocin analogs can be designed that are extremely potent splanchnic vasoconstrictors. Further insight into these areas should provide basic information on the role of these peptides in circulatory homeostasis.