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  • 1
    Electronic Resource
    Electronic Resource
    Intracellular activities during volume regulation byNecturus gallbladder (1984)
    Springer
    The journal of membrane biology 78 (1984), S. 187-199 
    Details
    ISSN: 1432-1424
    Keywords: cell volume ; microelectrodes ; ion activities ; hypertonicity ; ouabain ; ion exchange ; ion transport ; electroneutral ; epithelial
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Necturus gallbladder epithelial cells regulate their volume after a change in solution osmolality. We determined the intracellular activities of Na, K and Cl when the mucosal bathing solution osmolality was increased 18% by the addition of mannitol. The gallbladder was mounted in a rapid flow chamber and punctured simultaneously with two single-barrelled microelectrodes. One electrode sensed membrane potential and the other was sensitive to the activity of Na, K or Cl. Cell volume measurements, made in previous studies utilizing quantitative light microscopy, indicated that hypertonicity of the mucosal bath first caused a cell shrinkage of 15% followed by volume readjustment. Some loss of Na, K and Cl was observed during shrinkage; subsequently during volume regulation, the intracellular quantities of all three ions increased. The loss of Na during the initial cell shrinkage could be blocked by ouabain and was therefore due to increased transport. K and Cl losses were probably related to the increase in their concentrations during shrinkage. The gain of Na, K and Cl during volume regulation was similar in magnitude to the loss of these solutes during cell shrinkage. The increase of Na, K and Cl during volume regulation accounted for about 60% of the increase of cell solutes during this period indicating that other solutes also contributed to the volume regulation response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01925967
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  • 2
    Electronic Resource
    Electronic Resource
    Feedback inhibition of NaCl entry inNecturus gallbladder epithelial cells (1984)
    Springer
    The journal of membrane biology 82 (1984), S. 95-104 
    Details
    ISSN: 1432-1424
    Keywords: NaCl cotransport ; Na/Ca exchange ; cell volume ; intracellular Na activity ; ouabain ; KCl transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary WhenNecturus gallbladder epithelium is treated with ouabain the cells swell rapidly for 20–30 minutes then stabilize at a cell volume 30% greater than control. The cells then begin to shrink slowly to below control size. During the initial rapid swelling phase cell Na activity, measured with microelectrodes, rises rapidly. Calculations of the quantity of intracellular Na suggest that the volume increase is due to NaCl entry. Once the peak cell volume is achieved, the quantity of Na in the cell does not increase, suggesting that NaCl entry has been inhibited. We tested for inhibition of apical NaCl entry during ouabain treatment either by suddenly reducing the NaCl concentration in the mucosal bath or by adding bumetanide to the perfusate. Both maneuvers caused rapid cell shrinkage during the initial phase of the ouabain experiment, but had no effect on cell volume if performed during the slow shrinkage period. The lack of sensitivity to the composition of the mucosal bath during the shrinkage period occurred because of apparent feedback inhibition of NaCl entry. Another maneuver, reduction of the Na in the serosal bath to 10mm, also resulted in inhibition of apical NaCl uptake. The slow shrinkage which occurred after one or more hours of ouabain treatment was sensitive to the transmembrane gradients for K and Cl across the basolateral membrane and could be inhibited by bumetanide. Thus during pump inhibition inNecturus gallbladder epithelium cell Na and volume first increase due to continuing NaCl entry and then cell volume slowly decreases due to inhibition of the apical NaCl entry and activation of basolateral KCl exit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870736
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    Paper (German National Licenses)
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