Chronic administration of erythropoietin (EPO) is associated with an increase in arterial blood pressure in patients and animals with chronic renal failure (CRF). Several mechanisms have been considered in the pathogenesis of EPO-induced hypertension. These include the possible role of the rise of hematocrit and erythrocyte mass, changes in production or sensitivity to endogenous vasopressors, alterations in vascular smooth-muscle ionic milieu, dysregulation of production or responsiveness to endogenous vasodilatory factors, a direct vasopressor action of EPO, and finally arterial remodeling through stimulation of vascular cell growth.