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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 395 (1982), S. 212-219 
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 395 (1982), S. 227-231 
    ISSN: 1432-2013
    Keywords: d-Lactate ; Benzoate ; Cinnamate ; Nicotinic acid ; Pyrazinoate
    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 was measured. This efflux can be divided into a Na+-dependent, saturable component flowing through the brush border and a Na+-independent non-saturable component flowing through the paracellular pathway. The inhibitory potency of benzoate and its analogs, of phenyl-substituted acetate-, propionate-and butyrate analogs, of cinnamate and analogs, of heterocyclic monocarboxylic acids and related compounds added to the perfusate in a concentration of 10 mmol/l was measured. It was found that 1. benzoate added in a concentration of 10 mmol/l to the luminal perfusate inhibits transport ofd-lactate, and the meta- and para-substituted analogs of benzoate inhibit in a fashion predicted by Hammett's theory. Side groups which withdraw electrons from the COOH group inhibit while substitutes who deliver electrons toward the reaction center do not. 2. Replacement of a hydrogen atom by a phenyl ring at the C2 atom of acetate, glycolate and glyoxylate does not change the inhibitory pattern of these substances ond-lactate transport. Replacement of a hydrogen atom on the C2 atom of propionate and lactate reduces the ability of these molecules to inhibitd-lactate transport. But replacement of a hydrogen atom at the C3 atom of propionate, pyruvate and lactate abolishes the inhibitory potency. Similarly the inhibitory potency decreases from butyrate 〉 2-phenylbutyrate 〉 3-phenylbutyrate 〉 4 phenylbutyrate. The latter two are actually no longer inhibitory. 3. Trans-cinnamate, cis-cinnamate (3-phenyl trans or cis acrylic acid) and 3-phenylpropiolate are also not inhibitory. But introduction of an electron attracting CN group on C2 atom of cinnamate evokes inhibitory potency. 4. The heterocyclic compounds nicotinic acid and pyrazinoic acid exert strong inhibition ond-lactate transport, while picolinic acid and isonicotinic acid exert only moderate inhibition. Nicotinic and pyrazinoic acid show also a secretory component in their transport behaviour. 5. If the COOH group of benzoate is replaced by a SO3H group (benzenesulfonic acid) or if a second ring is induced (1 or 2 naphthoic acid) the inhibitory potency is lost. 6. Amongst other organic anions which do not inhibitd-lactate transport are paraaminohippurate, urate, and taurocholate. The data indicate that a main determinant of the specificity of the Na+-dependent aliphatic aromatic monocarboxylic acid reabsorption system in the renal brush border is the electron density at the reaction center, i.e. the free carboxylic group. Furthermore, the size of the molecule and its hydrophobicity at one cell pole is limiting for its ability to react with the carrier.
    Type of Medium: Electronic Resource
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