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Hypotonic stress activates an intermediate conductance K super(+) channel in human colonic crypt cells

Aim:To investigate the effect of hypotonic stress on human colonic crypts cells in terms of ion channel activity and intracellular Ca super(2+) concentration. Methods:Single crypts were isolated from biopsies taken during colonoscopy. The patch clamp technique was used (in the cell-attached mode) to...

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Bibliographic Details
Published in:Acta physiologica Scandinavica 2004-12, Vol.182 (4), p.361-368
Main Authors: Sand, P, Anger, Aa, Rydqvist, B
Format: Article
Language:English
Online Access:Get full text
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Summary:Aim:To investigate the effect of hypotonic stress on human colonic crypts cells in terms of ion channel activity and intracellular Ca super(2+) concentration. Methods:Single crypts were isolated from biopsies taken during colonoscopy. The patch clamp technique was used (in the cell-attached mode) to observe the activity of ion channels during hypotonic stress. Calcium measurements were made using the fluophores Fluo 3 or 4. Results:The intermediate conductance (29 pS), Ca super(2+)-sensitive, K super(+) channel (also known as KCNN4) previously described () was seen in 54 of 149 patches (36%) when the crypts were bathed in normal extracellular solution (290 mOsm kg super(-1)). Forty-one patches could be used for further analysis. Activation of one or several 29 pS channels was seen in 15 of 41 patches (39%) after 30 s to 4 min of exposure to hypotonic solution (160 mOsm kg super(-1)). The open probability increased from 0.0043 in control solution to 0.44 at 5 min of hypotonic stress. When the crypts were exposed to hypotonic solution, an increase in intracellular Ca super(2+) could be seen. The increase in intracellular Ca super(2+) emanates mainly from intracellular stores. Conclusion:The 29 pS K super(+) channel takes part in volume regulation in human colonic crypt cells. The activation of this channel is mediated through an increase in intracellular Ca super(2+).
ISSN:0001-6772
1365-201X
DOI:10.1111/j.1365-201X.2004.01366.x