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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. 692-697 
    ISSN: 1432-1440
    Keywords: Kidney ; Urine concentration ; Volume regulation ; Potassium ; Bicarbonate ; Aldosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cells of the renal medulla regulate their volume by transmembrane ion movements when exposed to large changes in osmolality. Since renal cells in culture release KHCO3 in response to hypotonic stress [11], we investigated the effect of an acute water load on urinary KHCO3 excretion in 5 healthy individuals. Water diuresis was induced by the ingestion of 1.51 hypoosmolal fluid (22 mosm/kg H2O) over 15 min. The rate of urinary volume excretion increased from an initial value of 1.4 ml/min to 9.3 ml/min after 75 min. Urinary osmolality dropped from an initial value of 940±32 mosm/kg H2O to 74±4 mosm/kg H2O (n = 5). The decrease of osmolality was accompanied by the transient release of potassium and bicarbonate. Peak values of KHCO3 excretion were observed between 30 and 45 min after the onset of the experiment corresponding to the drop of urinary osmolality. The magnitude of renal potassium release correlated significantly (r=0.93; P 〈 0.05) with endogenous plasma aldosterone concentrations measured prior to the experiment in the 5 volunteers. We conclude that medullary epithelial cells release KHCO3 when exposed to hypotonic stress. The volume regulatory response is upregulated by aldosterone.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 533-539 
    ISSN: 1432-2013
    Keywords: MDCK-cells ; Aldosterone ; Na+/H+ exchange ; Cl−/HCO 3 − exchange ; Intercalated cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Experiments in dome epithelium of Madin-Darby canine kidney (MDCK) cells were performed to elucidate aldosterone action on acid-base transport. By means of pH-sensitive microelectrodes the pH of the dome fluid was measured while the apical plasma membrane was superfused. In the absence of HCO 3 − the dome fluid (facing the basolateral cell membrane) alkalinized in response to 10−7 mol/l aldosterone. Amiloride (10−3 mol/l) inhibited dome formation and pH recovery of the dome fluid from an extracellular acid load. In the presence of HCO 3 − dome fluid acidified in response to aldosterone. The stilbene derivative diisothiocyanate-stilbene-2,2′-disulphonic acid (DIDS) or removal of Cl− from the apical perfusate inhibited this dome acidification. In aldosterone-depleted MDCK monolayers HCO 3 − was actively accumulated in the dome fluid in contrast to aldosterone-supplemented cells. The results indicate that aldosterone stimulates both amiloride-sensitive Na+/H+ exchange and DIDS-sensitive Cl−/HCO 3 − exchange in the apical cell membrane of MDCK cells. In the absence of aldosterone the HCO 3 − extrusion process is localized in the basolateral membrane in series with apical Na+/H+ exchange, while in the presence of aldosterone Cl−/HCO 3 − is mainly localized in the apical membrane in parallel with Na+/H+ exchange. Cl− exits the cell through apical Cl− channels and is absorbed via the paracellular route.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 526-532 
    ISSN: 1432-2013
    Keywords: Aldosterone ; MDCK cells ; Dome formation ; Differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vectorial transport of salt and water in the Madin-Darby canine kidney (MDCK) cell line is indicated by the formation of domes when a monolayer is grown on an impermeable support. We investigated aldosterone-induced dome formation and evaluated the dome as an experimental model. Transepithelial dome resistance was about 80 Ωcm2 and constant when dome size exceeded 2 · 10−4 cm2. The relative ion conductances (expressed as transference numbers) across the dome epithelium were t Na∶t Cl∶t K= 0.64∶0.24∶0.06. They reflect the permeability properties of the paracellular shunt pathway tested at physiological concentrations of the individual ions. Aldosterone accelerated dome formation in serum-deprived MDCK monolayers. Prostaglandin E1 and transferrin were supportive but not essential for aldosterone-induced dome formation. After 72 h dome density was equal in monolayers cultured in serum-supplemented medium either in the presence or absence of mineralocorticoids. We conclude that aldosterone induces cell polarization in MDCK monolayers, leading to the formation of domes. The dome epithelium appears to be electrically isolated from the adjacent monolayer and can be studied by microelectrode techniques.
    Type of Medium: Electronic Resource
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