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This study was designed to compare the effects of prostaglandin synthesis inhibition on calculated preglomerular and postglomerular resistance in hypertensive patients with unilateral renal artery stenosis (RAS) and in patients with essential hypertension.Sixteen patients with suspected renovascular hypertension underwent renal angiography: eight had unilateral renal artery stenosis ≥ 70% and eight had normal angiograms or stenosis ≤ 40%. Radionuclide renography and 6 h urinary collection were performed twice for each subject, at baseline and after indomethacin administration. Levels of urinary vasodilatory prostaglandins were measured by specific radioimmunoassays. Visual image analysis was performed to determine the parenchymal transit time (PTT). The glomerular filtration rate (GFR) was calculated from the plasma clearance of [99mTc]-diethylenetriamine pentaacetic acid (DTPA). The preglomerular and postglomerular resistances were estimated according to Gomez's equations.The prostaglandin excretion decreased significantly after indomethacin administration both in RAS and in essential hypertension patients. The PTT increased from 230 ± 10 to 340 ± 40s in the stenotic kidney compared with the contralateral kidney and the kidneys of essential hypertension patients. The GFR was decreased both in stenotic and in contralateral kidneys (48 ± 4 to 37 ± 5 and 60 ± 4 to 52 ± 5 ml/min, respectively) but did not decline in the kidneys of essential hypertension patients. The preglomerular resistance increased both in stenotic and in contralateral kidneys, whereas it did not rise significantly in the kidneys of essential hypertension patients. The postglomerular resistance in stenotic and contralateral kidneys of RAS patients was not altered.Prostaglandins limit GFR decreases in RAS by preventing preglomerular constriction without interfering with postglomerular constriction. Thus, the action of vasoactive prostaglandins on preglomerular resistance might maintain renal function in the short term by limiting the fall in GFR in the stenotic kidney and by increasing the GFR in the contralateral kidney.