Research Article| Volume 76, ISSUE 3, P373-382, September 1970

The renal response to ureteral obstruction: A model for the study of factors which influence glomerular filtration pressure

  • John R. Jaenike
    Reprint requests: Dr. John R. Jaenike, Dept. of Medicine, University of Rochester School of Medicine and Dentistry, 260 Crittenden Blvd., Rochester, N. Y. 14620.
    From the Department of Medicine, University of Rochester School of Medicine and Dentistry Rochester, N. Y. U.S.A.
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  • Author Footnotes
    ∗ Dr. Jaenike is a recipient of Public Health Service Career Development Award 2-K3-HE-4526 from the National Heart Institute.
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      The relationship of glomerular filtration pressure to filtration rate has been examined under various experimental conditions in the rat. Unilateral ureteral obstruction, of 24 hours' duration, produces a marked reduction in filtration rate, measured after release of occlusion. This excretory lesion is associated with a reduction in glomerular filtration pressure. The relationship between filtration rate and pressure after release of obstruction closely resembles that observed in the normal kidney in which perfusion pressure is reduced by aortic constriction. The data indicate that the reduction in filtration pressure is the sole factor responsible for excretory failure after ureteral obstruction and that this lesion is characterized by an increase in preglomerular arteriolar resistance. This conclusion is supported by the observation that the intraarterial infusion of vasodilators, papaverine and acetylcholine, markedly augments filtration rate and pressure in the affected kidney. The effect of volume expansion with mannitol or albumin solutions has been studied in this lesion. Both produce a rapid and marked increase in filtration rate and pressure after release of obstruction. The effect of mannitol on filtration pressure appears to be manifest only in the free flow state, not when mannitol is given after ureteral clamping. This suggests that the action of mannitol is mediated by an intrarenal feedback mechanism responsive to changes in sodium delivery to the distal nephron. Although the precise mechanism involved in the pathogenesis of decreased filtration pressure after unilateral ureteral obstruction remains undefined, this appears to offer a simple and useful model for the study of physiologic and pathologic factors which affect glomerular filtration pressure.
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