Alterations in renal prostaglandins (PG) have been reported in hypertensive animals and in essential hypertension. Some alterations in the pattern of PG are more likely to be secondary to hypertension, whereas others may reflect a defective adaptation to the hypertensive state thus contributing to the rise in blood pressure. A major role for vasodilatory arachidonic acid (AA) metabolites is to modulate the effects of vasoconstrictor stimuli on renal vasculature and sodium excretion; thus, an alteration of this interplay may be responsible for some forms of experimental and human hypertension.