To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E 2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E 2 concentration in

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... l venous plasma from the stenotic kidney was 9.25 ±1.48 pg/ml, which was significantly higher (/?<0.01) than the concentration in the renal venous plasma from the normal kidney (4.97±1.02 pg/ml) or in the aortic plasma (2.59±0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E 2 correlated significantly with a renin ratio greater than 1.5 (r=0.8211, p<0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E 2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120±6 to 110±5 mm Hg,p<0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (/?<0.05) and in the renal vein of the stenotic kidney (/?<0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure. These data indicate that renal prostaglandin plays an important role in the augmented release of renal renin and the pathogenesis of hypertension in human renovascular hypertension. {Hypertension 1989;14:461-468) From the Division of Hypertension and Nephrology (M.I., M.K., S.A., Y.M., M.K., T.O.) and the Division of Radiology