Abstract
The effect of mannitol upon glomerular ultrafiltration was examined in hydropenic Munich-Wistar rats. Superficial nephron filtration rate (sngfr) rose from 32.0±0.9 nl/min/g kidney wt to 42.0±1.6 (P < 0.001) in eight rats. Hydrostatic pressure gradients acting across the glomerular capillary (ΔP) were measured in glomerular capillaries and Bowman's space with a servo-nulling device, systemic (πA) and efferent arteriolar oncotic pressures (πE) were determined by microprotein analysis. These data were applied to a computer-based mathematical model of glomerular ultrafiltration to determine the profile of effective filtration pressure (EFP = ΔP — π) and total glomerular permeability (LpA) in both states. Filtration equilibrium obtained in hydropenia (LpA ≥ 0.099±0.006 nl/s/g kidney wt/mm Hg) and sngfr rose because EFP increased from a maximum value of 4.2±1.1 to 12.8±0.5 mm Hg after mannitol (P <0.01). This increase was due to both increased nephron plasma flow and decreased πA. Computer analysis of these data revealed that more than half (>58%) of this increase was due to decreased πA, consequent to dilution of protein. Since EFP was disequilibrated after mannitol, LpA could be calculated accurately (0.065 ± 0.003 nl/s/g kidney wt/mm Hg) and was significantly lower than the minimum estimate in hydropenia.
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