Bidirectional active transport of thiosulfate in the proximal convolution of the rat kidney

1980 ◽  
Vol 387 (2) ◽  
pp. 127-132 ◽  
Author(s):  
K. J. Ullrich ◽  
G. Rumrich ◽  
S. Kl�ss
Keyword(s):  
Active Transport ◽  
Rat Kidney ◽  
Proximal Convolution

Effect of parathyroid hormone on renal tubular permeability

1976 ◽  
Vol 231 (5) ◽  
pp. 1401-1407 ◽  
Author(s):  
WB Lorentz
Keyword(s):  
Parathyroid Hormone ◽  
Active Transport ◽  
Intravenous Infusion ◽  
Rat Kidney ◽  
Tubular Transport ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Tubular Permeability

The effect of parathyroid hormone (PTH) on renal tubular permeability has been studied utilizing micropuncture techniques in the rat kidney. After microinjection into superificial nephrons during control conditions, inulin (98.8 +/- 2.7%) and mannitol (97.2 +/- 2.4%) recovery from the experimental kidney was essentially complete. During intravenous infusion of PTH, inulin (99.3 +/- 2.9%) recovery was again complete. Mannitol recovery decreased signficantly after both early-proximal (84.7 +/- 5.8%, P less than 0.001) and late-proximal (89.7 +/- 2.8%, P less than 0.001) injections. There was no loss of either mannitol or inulin following distal tubular injection. Late-proximal TF/P inulin ratios during control conditions were 2.10 +/- 0.20 and decreased insignificantly to 1.99 +/- 0.21 during PTH infusion. Late-proximal TF/P mannitol rations were 2.09 +/- 0.21 during control periods and during PTH infusion decreased significantly to 1.78 +/- 0.19 (P less than 0.001). These results indicate that PTH induces a change in proximal tubular permeability to a usually impermeable nonelectrolyte, mannitol. The effects of PTH on proximal tubular transport could be partially explained by this alteration in permeability, which would increase passive backflux of actively transported species and decrease net transport while having no effect on active transport.

scholarly journals Transport and metabolism of galactose in rat kidney cortex

1972 ◽  
Vol 129 (5) ◽  
pp. 1109-1118 ◽  
Author(s):  
Pamela D. McNamara ◽  
Stanton Segal
Keyword(s):  
Active Transport ◽  
Substrate Concentration ◽  
Rat Kidney ◽  
Linear Increase ◽  
Kidney Cortex ◽  
Galactose Metabolism ◽  
Rat Kidney Cortex ◽  
Cortex Slices ◽  
Active Transport System ◽  
Kidney Cortex Slices

1. Analysis of transport of d-galactose was complicated by metabolism of the compound but appeared to have two components: a substrate-saturable component and a diffusion component. At low substrate concentration (<1mm) active transport was observed. Accumulation of galactose was largely independent of Na+concentration. The apparent Km for this component was 0.2mm. At substrate concentrations above 1mm the active transport system appeared saturated and further increases in substrate concentration resulted in a linear increase in the rate of galactose accumulation, but no concentration gradient was formed. 2. d-[1-14C]Galactose (2mm) was metabolized to14CO2 by rat kidney-cortex slices incubated at 37°C, at the rate of 68nmol/h per 100mg of tissue. 3. Intracellular components from such incubations were separated into a neutral fraction, the only major labelled component being galactose, and a phosphorylated fraction. 4. Phosphorylated metabolites found in galactose-incubated slices increased with increasing substrate concentration and achieved a limiting value of 0.42mm after 60min of incubation. 5. Galactose uptake was inhibited by anaerobiosis, dinitrophenol and phlorrhizin. 6. Methyl α-d-glucoside and d-glucose partially inhibited galactose uptake only at ratios of 100:1. 7. The presence of pyruvate did not decrease galactose metabolism although it did decrease production of14CO2 from [1-14C]galactose. Gluconeogenesis occurred in the presence of pyruvate and14C from galactose was found in glucose. 8. Rat kidney-cortex slices metabolized 2mm-[1-14C]galactonate to14CO2 at a rate of 20nmol/h per 100mg of tissue.

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