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Abstract
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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Article info
Publication history
Accepted:
July 2,
1970
Received:
February 27,
1970
Footnotes
☆This work was supported by United States Public Health Service Grant HE 07966 from the National Heart Institute.
Identification
Copyright
© 1970 Published by Elsevier Inc.
