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  • Articles: DFG German National Licenses  (2)
  • 1980-1984  (2)
  • Adaptation, HCO 3 − transport  (1)
  • Electrolyte transport  (1)
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  • Articles: DFG German National Licenses  (2)
Material
Years
  • 1980-1984  (2)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 1165-1172 
    ISSN: 1432-1440
    Keywords: Epithelial transport ; Kidney ; Lactate transport ; Electrolyte transport ; Epithelialer Transport ; Niere ; Laktattransport ; Elektrolyttransport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Resorption bzw. Sekretion im proximalen Nierentubulus läuft einmal passiv auf dem parazellulären Weg, d.i. zwischen den Zellen hindurch, ab, zum anderen aktiv, transzellulär, durch die Zellen hindurch. Der transzelluläre aktive Transport ist in der Regel sekundär aktiv. Er verläuft gekoppelt an den Fluß von Na+-Ionen, wobei ein transzellulärer Gradient von Na+-Ionen, der seinerseits durch die kontraluminal gelegene (Na+-K+)-ATPase geschaffen wird, die Triebkraft liefert. Einmal in der Zelle, verlassen die Substanzen die kontraluminale Zellseite vermittels Karrier, die Na+-unabhängig sind. Mit Hilfe von Mikroperfusions- und elektrophysiologischen Techniken sowie mit Hilfe von Bürstensaumvesikeln wurde der Na+-Kotransport von Aminosäuren, Phosphat, Sulfat, Thiosulfat, Gallensäuren, aliphatischen und aromatischen Monokarboxylsäuren (Laktat) sowie der von Dikarboxylsäuren untersucht. Besonderes Augenmerk wurde dem bidirektionalen Transport von Thiosulfat sowie der Spezifität des Mono- und Dikarboxylsäure-Transportsystems gewidmet.
    Notes: Summary The transport through the epithelial cell layer of the renal proximal tubule proceeds in principle by passive paracellular and active transcellular transport. The active transcellular transport is mostly secondary active. This means it proceeds coupled with the flux of Na+ ions, where-by the transcellular gradient of sodium, created by the (Na++K+)-ATPase, located at the contraluminal cell side, provides the main driving force. Once in the cell the substances leave the other cell side by a Na+-independent, but carrier-mediated transport system. Using microperfusion and electrophysiological techniques as well as brush border membrane vesicle preparation the Na+-H+ countertransport and the Na+-cotransport of amino acids, phosphate, sulfate, thiosulfate, bile acids, aliphatic-aromatic monocarboxylic acids (lactate) and dicarboxylic acids was studied. Special emphasis will be given to the bidirectional transport of thiosulfate as well as to the specificity of the monocarboxylic acid and dicarboxylic acid transport system.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 389 (1981), S. 271-275 
    ISSN: 1432-2013
    Keywords: Adaptation, HCO 3 − transport ; Glycodiazine transport ; Metabolic acidosis ; Metabolic alkalosis ; Acetazolamide ; SITS ; Potassium deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using the technique of capillary perfusion and simultaneous luminal stop flow microperfusion the reabsorption of bicarbonate and glycodiazine from the papillary collecting duct was evaluated. Starting with equal H14CO 3 − and3H-glycodiazine concentrations in the luminal and peritubular perfusates, the decrease in the luminal concentration at 10 and 45 s contact time was measured. In control rats with 25 mmol/l HCO 3 − in the perfusates the rate of HCO 3 − reabsorption calculated from the 10 s values was 0.34 nmol cm−2s−1. In acute metabolic acidosis, the rate of bicarbonate reabsorption was 2,3 times higher. In metabolic alkalosis, the rate of bicarbonate absorption dropped to 13% of the control values. Also the 45 s values of acidotic and alkalotic animals differed significantly from each other. With 25 mmol/l glycodiazine in both perfusates the rate of biffer reabsorption as calculated from the 10 s values was 0.76 nmol cm−2s−1 in control rats and did not deviate significantly from this value in acidotic and alkalotic animals. In control rats the bicarbonate reabsorption in % was the same, no matter whether both luminal and capillary perfusate contained 25 mmol/l bicarbonate or 10 mmol/l. In acidotic rats the rate of HCO 3 − reabsorption did not change significantly if all Na+ in the perfusates was replaced by choline (0.88 versus 0.79 nmol cm−2s−1 at 25 mmol/l HCO 3 − ). When in acidotic rats 0.1 mmol/l acetazolamide or 1 mmol/l SITS (4-acetamido-4′-isothiocyanatostilbene-2,2′-disulfonic acid) was added to both perfusates the rate of HCO 3 − reabsorption dropped by 75 and 58%, respectively. A potassium deficient diet for one week and DOCA administration had no influence on the bicarbonate reabsorption of rats which were on standard diet. The data indicate that (1) the buffer reabsorption from the papillary collecting duct is rather due to H+ ion secretion than to buffer anion reabsorption. (2) The adaptation to metabolic acidosis and alkalosis is specific for bicarbonate and not seen with glycodiazine. (3) Within the concentration range tested the HCO 3 − reabsorption rises linearly with the HCO 3 t- concentration. (4) The HCO 3 − reabsorption in the papillary collecting duct is Na+-independent, it can be inhibited by acetazolamide and SITS, but is not influenced by K+-deficient diet plus DOCA.
    Type of Medium: Electronic Resource
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