Glomerular filtration response to elevated ureteral pressure in both the hydropenic and the plasma-expanded rat.
- 1 December 1975
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 37 (6), 819-829
- https://doi.org/10.1161/01.res.37.6.819
Abstract
The factors affecting glomerular ultrafiltration with elevated ureteral pressure were examined in both plasma-expanded (2.5% body weight) and hydropenic Munich-Wistar rats. Elevated ureteral pressure (20 mm Hg) alternated as the initial condition in both groups. Glomerular capillary hydrostatic pressure (PG) and Bowman's space pressure (Pt) were measured directly in surface glomeruli with a servonulling device (deltaP = PG - PT), systemic (piA) and efferent (piE) peritubular capillary oncotic pressures were estimated by microprotein methods, and single-nephron glomerular filtration rates (sngfr) were determined by micropuncture techniques under control ureteral pressure and after increased ureteral pressure in both experimental groups. All data were then applied to equations describing the process of glomerular ultrafiltration to define the profile of effective filtration pressure (EFP = deltaP - pi) and the glomerular permeability coefficient (LpA), where sngfr = LpA-EFP. In plasma-expanded rats, sngfr fell from 44.8 +/- 2.2 to 38.5 +/- 1.5 nilters/min g-1 kidney weight (P less than 0.025) with elevated ureteral pressure entirely as a result of a decrease in the hydrostatic pressure gradient (deltaP), since PG did not rise and nephron plasma flow remained constant. In hydropenic rats, sngfr fell from 34.7 +/- 1.6 to 27.3 +/- 1.6 nliters/min g-1 kidney weight with increased ureteral pressure. PG rose 8.7 mm Hg (P less than 0.001) due to an increase in vascular resistance between the peritubular capillaries and the renal vein which prevented the reduction in deltaP. The reduction in sngfr appeared to result from a reduction in LpA resulting in disequilibration of EFP. Nephron plasma flow was not changed. The filtration response to elevated ureteral pressure was modified by the prior state of volume expansion and was not associated with changes in either nephron blood flow or afferent arteriolar resistance.This publication has 16 references indexed in Scilit:
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