Prostaglandin I 2 /E 2 Ratios in Unilateral Renovascular Hypertension of Different Severities

Abstract

Differences between prostaglandins I 2 and E 2 in their renal synthesis and pathophysiological roles were investigated in unilateral renovascular hypertension of different severities in 18 patients: 6 with mild stenosis (<75% of the diameter) of the renal artery, 7 with moderate stenosis (75% to 90%), and 5 with severe stenosis (>90%). Before and after aspirin administration (10 mg/kg), renal venous and aortic plasma was assayed for 6-ketoprostaglandin F 1α (instead of prostaglandin I 2 ), prostaglandin E 2 , and renin activity. In mild or moderate stenosis, the mean 6-ketoprostaglandin F 1α level in renal venous plasma from the stenotic side was not different from that from the normal side or from aortic plasma. Prostaglandin E 2 levels and renin activity in such patients were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited prostaglandin E 2 synthesis and suppressed renin release from stenotic kidneys and lowered blood pressure as the renin activity decreased in patients with mild or moderate stenosis. In severe stenosis, levels of 6-ketoprostaglandin F 1α and prostaglandin E 2 were higher on the stenotic side than on the normal side and higher in venous than in aortic plasma. Aspirin inhibited the synthesis of both prostaglandins and suppressed renin release from the stenotic kidney. In patients with unilateral renovascular hypertension with mild or moderate stenosis of the renal artery, prostaglandin E 2 , rather than I 2 , seems to contribute to further acceleration of renin release. Prostaglandin I 2 may increase and participate in further renin release when the stenosis is severe.