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SUMMARY In a group of six patients diagnosed as having unilateral renovascular hypertension due to fibromuscular dysplasia, inulin glomerular filtration rate, (GFR) and PAH renal plasma flow, (RPF) clearances, urine flow (V), urine sodium (UV Nl ), potassium (UV K ), urinary excretion of prostaglandin E^ (UV reEj ), thromboxane B 2 (UV TxJ , 2 ), and 6-keto prostaglandin F la (UV^^) were measured in each kidney before and after the i.v. administration of furosemide (20 mg). The basal values of GFR, RPF, UV Ni , UVpc E ,, UV TlB ,, and UV 6 . krto . PCFla were lower (p < 0.01) in the stenotic kidney. Furosemide increased RPF 11 % and 50%, GFR 25% and 62%, and V 142% and 280% in the contralateral and stenotic kidney respectively. The increase of UV Na was similar in the two kidneys. In the stenotic kidney, both UVpcEj and UVj^^pcf^ increased significantly (p < 0.01) with furosemide while UV TlB , remained unchanged. Furosemide did not alter the rate of excretion of the three prostaglandins measured in the contralateral kidney. We conclude that furosemide significantly improves renal circulatory and excretory function of the stenotic kidney. Since prostaglandin excretions also increased, the vasodilatation in the stenotic kidney may be prostaglandin mediated. IT is known that the vasodilator action of furosemide in the normal kidney is mostly mediated by increased synthesis of prostaglandins, 1 " 4 which may also modulate the diuretic effects of furosemide. 4 Furosemide is currently used in patients with unilateral renovascular stenosis; however, it is not known whether its hemodynamic and diuretic effects are equally exerted or predominantly exerted in the stenotic kidney or in the contralateral kidney. Further, we have no knowledge about the changes induced by furosemide in prostaglandin synthesis in the stenotic and contralateral kidney. 56 In a recent survey of the literature, 7 there is convincing evidence supporting the notion that increased synthesis of prostaglandins is important inFrom the Departments of Nephrology and Endocrinology, 1st October and Ramon y Cajal Hospitals, Madrid, Spain, and from the Departments of Nephrology and Physiology, Mayo Clinic and Foundation, Rochester, Minnesota.Supported by Grant HL16496 from the National Institutes of Health, the National Heart, Lung and Blood Institute, and grants from the Mayo Foundation and the Spanish Ministry of Health (FIS Exp. 83/0575).Address for reprints: Dr. J.C. Romero, Department of Physiology, 9th Floor Guggenheim Building, Mayo Foundation, Rochester, Minnesota 55905. the maintenance of renal blood flow during the early phases of renovascular hypertension. However, in the chronic stages of hypertension, the role of prostaglandins has not been adequately explored. 7This study was undertaken to determine the effect of furosemide on renal hemodynamics, renal excretory function, and postaglandin excretion in both the stenotic apd contralateral kidneys of patients with renovascular hypertension. Materials and Methods Patient ProtocolThe study was co...

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In a group of 26 patients diagnosed as essential hypertensive (EH) and in a control group (CG) of 27 normotensive volunteers the urinary excretion of PGE2, plasma renin activity (PRA) and plasma aldosterone were measured. EH patients were classified into normoreninemic (NREH) (n = 21) and hyporeninemic (LREH) (n = 5) by the response of PRA to the combined stimuli of ambulation and furosemide. Urinary PGE2 excretion was higher in NREH than in CG (p less than 0.05) while LREH showed values lower than in CG (p less than 0.001). Plasma aldosterone levels were similar in the three groups. In CG and EH patients PRA and urinary PGE2 were closely related (CG r = 0.516, p less than 0.05, EH patients r = 0.674, p less than 0.001). Indomethacin administration induced a decrease of PGE2 in both CG (n = 8) and NREH (n = 8) (p less than 0.01). In contrast, indomethacin induced no changes in PGE2 excretion of LREH (n = 5). Furthermore in the group of patients with NREH indomethacin induced a significant increase in blood pressure (p less than 0.01) and body weight (p less than 0.01) while glomerular filtration rate, 24 hour natriuresis PRA and plasma aldosterone decreased (p less than 0.01). On the contrary, in LREH indomethacin did not alter any of the parameters measured. These results indicate that LREH and NREH may be regarded as two different populations distinguishable not only by different secretion of PRA but also by different excretion of PGE2 in urine and by their characteristic response to indomethacin.