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Research Article Free access | 10.1172/JCI107324
Department of Medicine, Veterans Administration Hospital, San Francisco, California 94121
Department of Medicine, University of California, San Francisco, California 94122
Department of Chemical Engineering, Stanford University, Stanford, California 94305
Find articles by Deen, W. in: JCI | PubMed | Google Scholar
Department of Medicine, Veterans Administration Hospital, San Francisco, California 94121
Department of Medicine, University of California, San Francisco, California 94122
Department of Chemical Engineering, Stanford University, Stanford, California 94305
Find articles by Troy, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Veterans Administration Hospital, San Francisco, California 94121
Department of Medicine, University of California, San Francisco, California 94122
Department of Chemical Engineering, Stanford University, Stanford, California 94305
Find articles by Robertson, C. in: JCI | PubMed | Google Scholar
Department of Medicine, Veterans Administration Hospital, San Francisco, California 94121
Department of Medicine, University of California, San Francisco, California 94122
Department of Chemical Engineering, Stanford University, Stanford, California 94305
Find articles by Brenner, B. in: JCI | PubMed | Google Scholar
Published June 1, 1973 - More info
Pressures and flow rates were measured in accessible surface glomeruli of mutant Wistar rats under conditions deliberately designed to prevent achievement of filtration pressure equilibrium, that is, the equalization of transcapillary hydrostatic and oncotic pressures by the efferent end of the glomerulus as typically observed in the normal hydropenic rat. Disequilibrium was obtained at elevated levels of glomerular plasma flow (GPF) brought about by acute expansion of plasma volume with a volume of rat plasma equal to 5% of body weight. Glomerular hydrostatic and oncotic pressures measured at high GPF were used to calculate the ultrafiltration coefficient, Kf, the product of effective hydraulic permeability and surface area. GPF was then either lowered (by aortic constriction) or raised (by carotid occlusion) in order to examine the dependence of Kf on GPF. The value of Kf per glomerulus, 0.08 nl/(s·mm Hg), was found not to vary over an approximately twofold range of GPF. This finding, taken together with data from previous studies from this laboratory, leads us to conclude that plasma-flow dependence of glomerular filtration rate (GFR) results primarily from flow-induced changes in mean ultrafiltration pressure, rather than large changes in Kf.