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  • 1
    Electronic Resource
    Electronic Resource
    Contraluminal transport of small aliphatic carboxylates in the proximal tubule of the rat kidney in situ (1986)
    Springer
    Pflügers Archiv 407 (1986), S. 488-492 
    Details
    ISSN: 1432-2013
    Keywords: Lactate ; Pyruvate ; 3-hydroxybutyrate ; Acetoacetate ; Nonspecific anion channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to study the characteristic of contraluminal transport of hydrophylic small fatty acids the in situ stopped flow microperfusion technique [12] has been applied. By measuring with 4 s contact time the decrease in the contraluminal concentration of the respective radiolabelled substances the concentration dependence of the influx into the cortical cells was tested. The 4 s decrease in contraluminal concentration of chloroacetate,l-lactate,d-lactate, 3-hydroxybutyrate and acetoacetate was between 26% and 31%. For each substance the percent decrease was the same, no matter whether it was offered in a concentration of 0.1 or 10 mmol/l. Contraluminal disappearance of 0.1 mmol/ll-lactate was not influenced by 5 mmol/l H2DIDS, probenecid, phloretin, mersalyl or cyanocinnamate, but it was significantly (37%) inhibited by 5-nitro-2-(phenyl-propyl-amino) benzoate, a blocker of the nonspecific anion channel. The percent decrease in propionate uptake was somewhat larger — between 36% and 39% — but again not different at 0.01, 0.1, 1.0 and 10 mmol/l. With pyruvate the contraluminal decrease was 20% at 0.1 mmol/l and 31% at 10 mmol/l. The percent disappearance of the aromatic pyrazinoate was 38% and 34% at 0.1 and 10 mmol/l and for nicotinate 42% and 22%, respectively. The disappearance of nicotinate (0.1 mmol/l) was significantly inhibited by 10 mmol/l pyrazinoate and paraaminohippurate (PAH). The data are in agreement with the hypothesis that the hydrophilic small fatty acids traverse the contraluminal cell side by simple diffusion, possibly via the unspecific anion channel [14], pyruvate via the dicarboxylic acid pathway in a cooperative manner and pyrazinoate, as well as nicotinate, via the PAH pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00657505
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  • 2
    Electronic Resource
    Electronic Resource
    Bicarbonate reabsorption in the papillary collecting duct of rats (1981)
    Springer
    Pflügers Archiv 389 (1981), S. 271-275 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00584789
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  • 3
    Electronic Resource
    Electronic Resource
    Reabsorption of monocarboxylic acids in the proximal tubule of the rat kidney (1982)
    Springer
    Pflügers Archiv 395 (1982), S. 212-219 
    Details
    ISSN: 1432-2013
    Keywords: SITS ; Probenecid ; Phloretin ; Acetazolamide ; Lactate ; Renal tubule
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The transport ofd-lactate across the epithelium of the late proximal convolution was investigated by two methods: 1. by measuring the zero net flux transtubular concentration difference (Δc tt,45s) and the permeability (P) ofd-lactate and calculating from both the transtubular active transport rate (J lac act ). 2. By measuring the 3.5 s efflux ofd-lactate from the tubular lumen, while blood was flowing through the capillaries. The 3.5 s efflux comprises two components, one going through the brush border (J lac bb ) and one going the paracellular pathway (J lac paracell =P lac·c lac lumen). Both,J lac act andJ lac bb ofd-lactate gave the sameK m 1.9 and 1.7 mmol/l and the same maximal transport rate 3.2 and 2.9 pmol cm−1 s−1. TheK i ofl-lactate tested againstJ lac act andJ lac bb ofd-lactate was also the same: 1.1 and 1.0 mmol/l. These data indicate that under our experimental conditions only the flux through the brush border seems to be rate limiting and thatd-lactate uses the same transport system asl-lactate. When Na+ was omitted from the perfusatesJ lac act disappeared completely, whileJ lac bb was reduced by 64%. These data reflect the Na+ dependence of thed-lactate transport through the brush border. Variation of intra-and extracellular pH by raisingpCO2, omitting HCO 3 − from the perfusates or adding acetazolamide had no effect on the transport ofd-lactate when α-ketoglutarate was used as fuel. However, when acetate was used as fuel, intracellular acidosis brought the reducedJ lac act back to the values obtained with α-ketoglutarate as fuel. It is suggested that this is an effect on a contraluminal transport step. Probenecid (5 mmol/l) and phloretin (0.25 mmol/l) inhibitedJ lac act significantly.J lac bb , however, was only inhibited by probenecid when acetate was used as fuel. These data indicate that both compounds act on thed-lactate exit at the contraluminal cell side, but that probenecid acts in addition at the luminal cell side. SITS (1 mmol/l) augmentedJ lac bb when acetate was used as fuel and is similar to the effect of lowering intracellular pH as described above. The SH reagents mersalyl (1.0 mmol/l) and maleolylglycine (1 mmol/l) did not influenceJ lac bb .
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584812
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  • 4
    Electronic Resource
    Electronic Resource
    Reabsorption of monocarboxylic acids in the proximal tubule of the rat kidney (1982)
    Springer
    Pflügers Archiv 395 (1982), S. 220-226 
    Details
    ISSN: 1432-2013
    Keywords: Na+-dependent transport ; d-Lactate transport ; Small fatty acids ; 3-Hydroxybutyrate ; Acetoacetate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The 3.5 s efflux ofd-lactate (1 mmol/l) injected in the lumen of the late proximal convolution as well as the zero net flux transtubular concentration difference ofd-lactate, which is a measure of its active transtubular transport rate, were determined. The inhibitory potency of small fatty acids and their analogs added to the perfusate in a concentration of 10 mmol/l on both, the 3.5 s efflux and in most cases also the 45 s transtubular concentration difference ofd-lactate was measured. It was found that 1. small fatty acids from acetate to octanoate inhibit 3.5s efflux ofd-lactate, the largest inhibition being exerted by propionate and butyrate. With increasing chain length the inhibitory potency decreased and disappeared with decanoate. 2. Considering the acetate-, propionate- and butyrate analogs, introduction of an electron attracting group such as Cl, Br, I, CN, SH, N3 on C atom 2 increased the inhibitory potency, compared to the unsubstituted fatty acid. An OH on C2 increased or did not change the inhibition while an OH on C atom 3 reduced or blunted the inhibition. A keto-group, as it is present in glyoxylate prevented inhibition, but pyruvate inhibited to the same extent as lactate, and acetoacetate was even more inhibitory than 3-hydroxybutyrate. Cl substitution on C3 preserved the strong inhibitory potency, while 4-Cl butyrate, was only sparsely inhibitory. A NH 3 + group at any position precludes inhibition. 3. As seen with Cl or OH substituted propionate and butyrate the inhibitory potency increased with decreasingpK a of the compounds. 4. Increasing the chain length by a CH3 as from acetate to propionate, from glycolate to lactate and also from glyoxylate to pyruvate increased the inhibitory potency. 5. When tested against the 3.5 s efflux ofl-lactate, the same inhibitory pattern was seen as withd-lactate. 6. The transport of chloroacetate, glycolate and acetoacetate, which were available in a radio-labeled form of high specific activity, was measured directly in 3.5 s efflux studies. It was Na+-dependent and could be inhibited by 10 mmol/ll-lactate. Glyoxylate, on the other hand, which did not inhibitd-lactate transport, did also not show a Na+-dependent,l-lactate inhibitable efflux from the tubular lumen. The data indicate that a variety of short chain fatty acids and their analogs are transported by the same Na+-dependent transport system in the brush border which transportsl- andd-lactate. The specificity is determined by the molecule size, hydrophobicity of one part of the molecule, the electron attracting abilities of substitutes on C-atom 2 or 3 and the charge distribution on the molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584813
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  • 5
    Electronic Resource
    Electronic Resource
    Coupling between proximal tubular transport processes (1977)
    Springer
    Pflügers Archiv 368 (1977), S. 245-252 
    Details
    ISSN: 1432-2013
    Keywords: Renal tubule ; H+ ion secretion ; Na+ coupled transport ; Ouabain ; SITS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The rate of active transport by the proximal renal tubule of amino acid (l-histidine), sugar (α-methyl-d-glycoside), H+ ions (glycodiazine), phosphate and para-aminohippurate was evaluated by measuring the zero net flux concentration difference (Δc) of these substances. In the case of calcium the electrochemical potential differenceΔc +zFci Δϕ/RT) was the criterion employed. The rate of isotonic Na+-absorption (JNa) was measured with the shrinking droplet method. The effect of ouabain on the transport of these substances was tested in the golden hamster and the effect of SITS (4-acetamido-4′isothiocyanatostilbene 2,2′-disulfonic acid) was observed in rats. Ouabain (1 mM) applied peritubularly incompletely inhibited JNa (80%), but in combination with acetazolamide (0.2 mM) the inhibition was almost complete (93%). In addition, ouabain inhibited the sodium coupled (secondary active) transport processes ofl-histidine, α-methyl-d-glycoside, calcium and phosphate by more than 75%. It did not affect H+ (glycodiazine) transport and PAH transport was only slightly affected. When SITS (1 mM) was applied from both sides of the cell it inhibited H+ (glycodiazine) transport by 72% and reduced JNa by 38% when given from only the peritubular cell side. SITS (1 mM), however, had no significant affect on H+ secretion and sodium reabsorption if it was applied from only the luminal side. Furthermore it had no affect on the other transport processes tested, regardless of the cell side to which it was applied. When the HCO 3 − buffer or physically related buffers were omitted from the perfusate the absorption of Na+ was reduced by 66%, phosphate by 44%, andl-histidine by 15%. All the other transport processes tested were not significantly affected. The data are consistent with the hypothesis that the active transport processes of histidine, α-methyl-d-glycoside and phosphate, which are located in the brush border, are driven by a sodium gradient which is abolished by ouabain. This may also apply to the Na+-Ca2+ countertransport located at the contraluminal cell side. The residual Na+ transport remaining in the presence of ouabain is likely to be passively driven by the continuing H+ transport which probably is driven directly by ATP. SITS seems to inhibit the exit step of HCO 3 − from the cell and secondary to that, the luminal H+-Na+ exchange and consequently the Na+ reabsorption. In the absence of HCO 3 − buffer in the perfusates the luminal H+-Na+ exchange seems to be affected and the pattern of inhibition of the other transport processes is almost the same as with SITS. The different effects onP i reabsorption observed under these conditions might be explained by possible variations in intracellular pH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585203
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