Renal extraction ratios and plasma-binding studies of radioiodinated o-iodohippurate p-aminohippurate in man.
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Biomedical subjects
Publications and source records attributed to C G Strong.
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Forty hypertensive patients were studied to examine the assumption that the angiotensin pressor dose reflects endogenous renin activity. Peripheral renin activity was assayed by the method of Boucher et al.(4) Sensitivity to the infusion of synthetic angiotensin II was determined as suggested by Kaplan and Silah.(1)Sixteen patients with essential hypertension with normal renal angiography required 3.8 ng. angiotensin/kg./min. to raise the diastolic pressure 20 mm. Hg. All but one were sensitive to angiotensin infusion of less than 5 ng./kg./min. Renin activity was normal in all except in one sensitive subject. Angiotensin infusion response and mean renin activity in 13 patients with essential hypertension with abnormal renal angiography were similar to that of the first group. The pressor dose in 11 renovascular hypertensives was 9.8 ng./kg./min. All but three had elevated plasma renin activity.OUR RESULTS SUGGEST THAT: (1) the angiotensin infusion test is suitable for differentiating patients with true renovascular hypertension from those with essential hypertension with or without associated renal artery disease; (2) the angiotensin pressor dose correlates with the level of peripheral venous renin activity (p < 0.01).
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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 (UVNa), potassium (UVK), urinary excretion of prostaglandin E2 (UVPGE2), thromboxane B2 (UVTxB2), and 6-keto prostaglandin F1 alpha (UVPGF1 alpha) were measured in each kidney before and after the i.v. administration of furosemide (20 mg). The basal values of GFR, RPF, UVNa, UVPGE2, UVTxB2, and UV6-keto-PGF1 alpha were lower (p less than 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 UVNa was similar in the two kidneys. In the stenotic kidney, both UVPGE2 and UV6-keto-PGF1 alpha increased significantly (p less than 0.01) with furosemide while UVTxB2 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.