Angiotensin II and norepinephrine promote formation of prostaglandins (PG), e.g., PGE2 and PGI2, that are capable of counteracting the vasoconstrictor actions of these pressor hormones. During activation of the renin-angiotensin and/or the sympathetic nervous systems, the administration of prostaglandin synthesis inhibitors causes vasoconstriction in renal and probably in extrarenal vasculatures, which suggests that antagonism of vasoconstrictor systems by prostaglandins is a feature of processes controlling arterial vascular tone. It follows, then, that endogenous prostaglandins may contribute to the regulation of blood pressure by opposing hormone-induced vasoconstriction. This implies that an uncompensated reduction in prostaglandin synthesis could cause blood pressure to rise. However, reports that prostaglandin synthesis inhibitors cause elevation of blood pressure conflict with reports that they do not. Obscuring the interpretation of such studies is the fact that inhibitors of prostaglandin synthesis also lower plasma renin activity, which may offset any tendency of blood pressure to rise consequent to reduced synthesis of antihypertensive prostaglandins. Hence it is premature to draw any firm conclusion regarding the full extent of the contribution of prostaglandins to blood pressure control. Nonetheless, the reviewed evidence commands consideration of the antagonism of the action of vasoconstrictor hormones by one or more prostaglandins as a feature of antihypertensive mechanisms.