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Research Article Free access | 10.1172/JCI107250
Department of Physiology, University of Munich, Munich, West Germany
Department of Physiology and Medical Biophysics, University of Uppsala, Uppsala, Sweden
Find articles by Schnermann, J. in: JCI | PubMed | Google Scholar
Department of Physiology, University of Munich, Munich, West Germany
Department of Physiology and Medical Biophysics, University of Uppsala, Uppsala, Sweden
Find articles by Persson, A. in: JCI | PubMed | Google Scholar
Department of Physiology, University of Munich, Munich, West Germany
Department of Physiology and Medical Biophysics, University of Uppsala, Uppsala, Sweden
Find articles by Ågerup, B. in: JCI | PubMed | Google Scholar
Published April 1, 1973 - More info
The present experiments were performed to quantify the effect of changes in distal tubular sodium delivery on glomerular flow dynamics both below and above the normal physiologic range. Glomerular capillary pressure as derived from the tubular stop flow pressure was assessed while the loop of Henle of the same nephron was perfused with varying flow rates. During Ringer perfusion no change of glomerular capillary pressure was observed when flow was increased from 0 to 13 nl/min. Further increasing flow to 27 nl/min was associated with a reduction of glomerular hydrostatic pressure by an average of 7.0±4.4 cm H2O (±SD). During perfusion at a rate of 43 nl/min glomerular pressure was decreased by a mean of 10.5±4.0 cm H2O. Changing the flow rate in small steps revealed that a significant reduction of capillary pressure was found when increasing the flow rate from 13 to 21 nl/min and that the maximum response was reached at 32 nl/min. No effect of perfusion rate changes on glomerular capillary pressure was observed when 300 mM mannitol was used as perfusion fluid. These results imply that a nonlinear relationship exists between end-proximal flow rate and glomerular capillary pressure. It is suggested that during deviations of distal sodium delivery into a positive direction filtration rate is intrarenally regulated probably by prevalence of afferent arteriolar constriction. During reductions of distal sodium load intrarenal regulation is either abolished or it involves proportionate resistance changes of both afferent and efferent arterioles.