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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Inst. and Methods in Physics Research, B 63 (1992), S. 227-230 
    ISSN: 0168-583X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Chromatography B: Biomedical Sciences and Applications 233 (1982), S. 432-436 
    ISSN: 0378-4347
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 361 (1975), S. 61-64 
    ISSN: 1432-2013
    Keywords: H+ transport ; HCO 3 − ATPase ; Acidosis ; Alkalosis ; Salivary duct
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An ATPase stimulated by HCO 3 − ions and other oxybases and inhibited by SCN− has been found in main exeretory duct of rat submaxillary gland, a tissue, capable of actively secreting HCO 3 t- ions. No such ATPase was found in the rabbit duct, which normally does not secrete HCO 3 − . The HCO 3 − ATPase was localized in the plasma membrane fraction of the homogenate, as evidenced by the marker 5′-nucleotidase. The activities of the HCO 3 − ATPase increased in metabolic alkalosis and decreased in metabolic acidosis in parallel to secretion of HCO 3 − and K+ ions by the duct epithelium. These findings provide further evidence that the membrane-bound HCO 3 − ATPase is involved in active H+/HCO 3 − transport.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 361 (1975), S. 55-59 
    ISSN: 1432-2013
    Keywords: Active secretion of K+ and HCO 3 − ; Active Na+ reabsorption ; Membrane conductance of Na+ and K+ ; Salivary duct ; Amiloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to elucidate whether or not active secretion of potassium and bicarbonate by the rat submaxillary duct epithelium operates independently of sodium reabsorption, Na+ transport was blocked by amiloride, which is known to inhibit Na+ entry from lumen into cell. With 10−4 M amiloride in HCO 3 − -Ringer at the luminal side, the transepithelial electrical potential difference approached zero, the Na+ conductance of the luminal cell membrane was drastically reduced, and the K+ conductance was significantly reduced. Net K+ secretion was reduced by 80%, whereas net HCO 3 − secretion was significantly increased. The remaining 20% of net K+ secretion proceeded at zero net Na+ transport and in the absence of significant chemical and electrical potential differences between lumen and interstitium of the duct. This active component of net K+ secretion was accompanied by an equal rate of active HCO 3 − secretion. These findings confirm the independence of this active secretion of K+ and HCO 3 − from Na+ transport. They indicate an electrically neutral secretion of K+ and HCO 3 − , probably by the postulated luminal K+−H+-exchange mechanism. The 80% of net K+ secretion, which were abolished by amiloride together with Na+ reabsorption, seem to be functionally coupled with Na+ transport. The linkage of K+-to-Na+ is probably mediated by a luminal carrier exchanging Na+ for K+ and H+.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 405 (1985), S. S67 
    ISSN: 1432-2013
    Keywords: Rat colon ; Short-circuit current ; Electrolyte transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A direct clamping technique is demonstrated, which allows monitoring of rapid changes of the short-circuit current (I sc) and the specific transepithelial resistance (R m) as well as measurement of ion fluxes under short-circuit conditions in vivo. Due to the cylindrical symmetry of the colon the intraluminal electrode was devised as a centrally fixed silver rod, by which radial current injection was achieved. The geometrical arrangement of the electrodes guaranteed zero potential difference (PD) along the whole axis of the colon segment. TheI sc was determined to 3.3±0.7 μeq h−1cm−2 andR m equal to 121±5 Ωcm2. These data obtained by direct short-circuiting agree well with our earlierR m andI sc data based on cable analysis, where theI sc was calculated from the open-circuit PD andR m. This is considered as evidence for the reliability of the two independent in vivo techniques. Their validity was confirmed by the expected effects of drugs acting on rheogenic ion transport. Both the indirect (viaR m) as well as the directI sc determination may be used alternatively as required; one may serve to match the other. For larger tubular structures like the rat colon the direct clamping should be prefered as the standard procedure for theI sc determination in vivo.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 292 (1976), S. 189-192 
    ISSN: 1432-1912
    Keywords: Amiloride ; Ouabain ; Active transport of Na+, K+, H+/HCO 3 - ; Membrane ATPases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The submaxillary duct epithelium, which actively transports Na+ (rabbit) and, in addition, K+ and H+/HCO 3 - (rat), was used as a model epithelium to compare the effects of ouabain and amiloride on transport parameters. 1. Ouabain was only effective from the interstitial side, amiloride, however, only from the luminal side. Amiloride induced effects on transport of the ions were seen within less than 1 s, ouabain effects, however, only after minutes. 2. Ouabain inhibited in a parallel fashion the Na+ transport potential and the Na+−K+-ATPase activity. It had no effect on the Mg2+-ATPase and the HCO 3 - -ATPase. 3. Amiloride also inhibited the Na+ transport potential and the Na+−K+-ATPase; however, the Na+ transport potential was significantly more sensitive to amiloride than the Na+−K+-ATPase. 4. Amiloride inhibited in a similar fashion the Na+−K+-ATPase, the Mg2+-ATPase and the HCO 3 - -ATPase, but did not influence active HCO 3 - secretion. 5. It is concluded that the amiloride induced effects on the membrane ATPases are non-specific.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Keywords: Salivary electrolytes ; Bartter's syndrome ; pseudo-Bartters syndrome ; Conn's syndrome ; Speichelelektrolyte ; Bartter-Syndrom ; Pseudo-Bartter-Syndrom ; Conn-Syndrom
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Im pilocarpinstimulierten Parotisspeichel wurde beim Bartter- (n=1), Pseudo-Bartter- (n=2) und Conn-Syndrom (n=2) die Konzentration der mono- und bivalenten Ionen als Funktion der Flußrate untersucht. Des weiteren wurde nach einem mathematischen Ansatz von Knauf und Frömter (1970) die gesamte aktive Na+-Rückresorption einer Parotis sowie die passive Leckpermeabilität des Gangsystems für Na+ berechnet. Führendes speichelchemisches Symptom desBartter- undPseudo-Bartter-Syndroms war eine Steigerung der aktiven K+-Sekretion, wobei der Normbereich um mehr als das Doppelte überschritten wurde. Die Na+-Reabsorption, die im Kontrollkollektiv mit 171±12 µ Äq/min berechnet wurde, verhielt sich unterschiedlich: leicht erniedrigt beim eehten Bartter-Syndrom, gering erhöht beim Pseudo-Bartter-Syndrom. Die flußratenbezogene Exkretion von Ca und z.T. auch Mg war bei allen Bartter-Kranken gesteigert. In ähnlicher Weise bestanden für die Anionen HCO − 3 und anorg. Phosphat deutlich erhöhte Werte. Im Unterschied zu diesen Befunden war der Elektrolyttransport beimConn-Syndrom durch eine exzessive Zunahme der Na+-Reabsorption gekennzeichnet. Trotz vermehrter Leckpermeabilität des Gangsystems wurde der Normbereich um den Faktor 2–3 überschritten. Die flußratenbezogene Konzentration von K+ und anorg. P war leicht, die des Ca stark erhöht. Erniedrigte Werte kennzeichneten die Bicarbonatsekretion — im Gegensatz zum Bartter-Syndrom. Aufgrund der qualitativen und quantitativen Differenzen in der Speichelchemie beider Krankheitsbilder ist es zweifelhaft, daß Aldosteron allein für den veränderten Elektrolyttransport beim Bartter-Syndrom verantwortlich ist.
    Notes: Summary In three patients, one with Bartter's syndrome and two with pseudo-Bartter's syndrome, the excretion pattern of mono- and divalent ions of the parotid saliva was studied as a function of flow rate. The results were compared with those observed in normal adults and in two patients with Conn's syndrome. In both Bartter's and pseudo-Bartter's syndromes, salivary K+ secretion was more than two times higher if compared with the corresponding flow rates. Other symptoms of the complex alterations of electrolyte transport in Bartter's and pseudo-Bartter's syndromes were the increased salivary excretion of calcium, magnesium, bicarbonate and inorganic phosphorus. Na+ reabsorption was slightly decreased in the patient with true Bartter's syndrome, and moderately increased in pseudo-Bartter's syndrome. The typical feature in the two patients with Conn's syndrome showed to be an excessive increase of salivary sodium reabsorption. The total amount of sodium actively reabsorbed by the duct system (J*ac), exceeded the normal range by about a factor of 2–3. Simultaneously, and in contrast to Bartter's syndrome, the flow-dependent concentrations of bicarbonate were markedly and those of magnesium slightly lower. The concentrations of potassium and inorganic phosphorus were moderately elevated, whereas those of calcium were markedly increased. Quantitative as well as qualitative differences in the salivary electrolyte patterns in these diseases provide strong arguments against an exclusive role of aldosterone in the pathogenesis of the electrolyte disturbances in Bartter's and pseudo-Bartter's syndrome. Experiments on human parotid glands clearly demonstrate that alterations of transepithelial electrolyte transport in this disease are not only confined to the different segments of the renal tubulus, but seem to be a symptom of a generalized disturbance of electrolyte transport.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1440
    Keywords: Ascites ; Liver cirrhosis ; Xipamide ; Spironolactone ; Furosemide ; Resistance to diuretics ; Fractional sodium excretion ; Side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a randomized prospective study the efficacy and side effects of xipamide versus the combination spironolactone/furosemide in the treatment of cirrhotic ascites were studied. Out of 27 patients four responded to a basic treatment consisting of salt and water restriction and one had to be excluded because of deterioration of kidney function. The remaining 22 patients were randomized to additional treatment with either 20 mg xipamide/day (group I) or 200 mg spironolactone/ day combined with 40 mg of furosemide every other day (group II). A response to treatment during the first 4 days was seen in 7 of 11 patients of group I versus only 3 of 11 patients in group II. In the latter group 7 of 11 patients finally responded after 8 days of treatment. Responsiveness to either diuretic treatment strongly depended on pretreatment fractional Na excretion, FENa. The resistance to diuretic treatment can be predicted by a FENa〈0.2%, and could be overcome by additional strategies known to reduce avid proximal Na reabsorption. Xipamide frequently induced hypokalemia, whereas hyperkalemia was seen following treatment with spironolactone/furosemide. Kidney function remained stable during either diuretic treatment.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 68 (1990), S. 692-698 
    ISSN: 1432-1440
    Keywords: Gemfibrozil ; Gastric antacids ; Absorption ; Elimination ; Biliary excretion ; Jaundice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The disposition of the lipid-lowering drug gemfibrozil was studied in patients with either renal (n= 8) or hepatic disease (n= 8) and compared to those of healthy volunteers (n= 6). Gemfibrozil was determined in plasma and urine by means of a HPLC method. Urine was also analyzed for gemfibrozil conjugates. Following oral administration of 900 mg gemfibrozil, maximal plasma levels of the parent drug were 46.1±15.8 μg/ml, attained after 2.2±1.1 h. In chronic renal failure and in liver cirrhosis the plasma concentrations of gemfibrozil did not significantly differ from that of controls except in those patients who were comedicated with antacids. These patients had significantly lower Cmax and AUC values. The elimination half-life of the drug was 1.5 h in controls, 2.4 h in renal failure, and 2.1 h in liver disease. In healthy volunteers, only 0.02 to 0.15% of the given dose was recovered in the urine as parent gemfibrozil, while conjugates made up 7–14%. In patients with renal failure also, only traces of parent gemfibrozil could be detected, and conjugates accounted for 0.5–9.8%. In those with liver disease, however, about 0.1–0.2% were recovered in urine as parent gemfibrozil and up to 50% as conjugates. Strikingly, the amount of excreted conjugates in the urine was positively correlated to the direct bilirubin plasma concentration. It can be concluded that the elimination of gemfibrozil is not significantly influenced by renal failure. However, comedication with antacids markedly reduced plasma disposition of the drug. Patients with severe liver disease excreted more conjugated gemfibrozil via the kidney than did healthy controls. Thus, transfer across the canalicular cell membrane to the bile duct, rather than drug metabolization, is primarily disturbed in liver disease. Gemfibrozil accumulation is unlikely to occur in either kidney or liver disease.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 54 (1976), S. 97-104 
    ISSN: 1432-1440
    Keywords: H+-secretion, stomach, kidney ; HCO 3 − -secretion, pancreas, salivary glands ; membrane-bound HCO 3 − -ATPase ; pathology of buffer transport ; H+-Sekretion, Magen, Niere ; HCO 3 − -Sekretion, Pankreas, Speicheldrüse ; membrangebundene HCO 3 − -ATPase ; Störungen des Puffertransportes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Dem aktiven Puffertransport, der an Magen und Niere zur H+-Sekretion, am Pankreas und Speicheldrüse zur HCO 3 − -Sekretion führt, ist eine ATP-Phosphohydrolase zugeordnet, die typischerweise durch HCO 3 − -Ionen stimuliert wird. Im Gegensatz zur (Na+-K+)-ATPase, dem Transportenzym des Na+-Transportes, benötigt dieses Enzym nurein Ion und ist Ouabain unempfindlich. Die HCO 3 − -ATPase ist an die Plasmamembran der einzelnen Epithelien gebunden, jedoch im Gegensatz zur (Na+-K+)-ATPase luminal lokalisiert. Das Enzym ändert seine Aktivität proportional zur Rate des aktiven Puffertransportes, was seine Bedeutung als Transportenzym unterstreicht. Es werden Krankheitsbilder des gestörten Puffertransportes aufgeziegt, bei denen möglicherweise der Defekt im HCO 3 − -ATPase-System zu suchen ist.
    Notes: Summary Active buffer transport, e.g. H+-secretion by stomach and kidney and HCO 3 − -secretion by pancreas and salivary glands, is linked with the presence of a HCO 3 − stimulated ATP-Phosphohydrolase. In contrast to (Na+-K−)-ATPase which is considered to be equivalent to the Na+ pump, the HCO 3 − -ATPase requires onlyone ion for activation and is insensitive to ouabain. The HCO 3 − -ATPase is found in the plasma membrane of the epithelia, but in contrast to the (Na+-K+)-ATPase it is located in the luminal cell border. The activity of the HCO 3 − -ATPase changes in parallel along with the rate of active buffer transport, a finding which underlines its importance as a transport enzyme. Several disorders of buffer transport are described which are possibly associated with a defect of the HCO 3 − -ATPase system.
    Type of Medium: Electronic Resource
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