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Hypertonicity-induced cation channels

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Whenever studied in a quantitative fashion, hypertonicity-induced cation channels (HICCs) are found to be the main mediators of regulatory volume increase. In most instances, these channels are either inhibited by amiloride (but insensitive to Gd3+ and flufenamate) or they are efficiently blocked by Gd3+ and flufenamate (but insensitive to amiloride). Of note, however, from two preparations so far a mixed type of pharmacology has also been reported. Whereas the ion selectivity of amiloride-sensitive HICCs has not been studied in much detail yet, amiloride-insensitive channels are either equally permeable to Na+, K+, Cs+ and Li+ but impermeable to N-methyl-d-glucamine (NMDG+) or they exhibit a permeability to Li+ and NMDG+ that amounts to some 50% when compared with that of Na+. Also in this respect, however, some peculiarities do exist. Concerning the actual molecular correlate, evidence was reported that HICCs may be related to the (amiloride-sensitive) epithelial Na+ channel and/or to transient receptor potential channels. Recent findings suggest that HICCs may contribute to cell proliferation, just as the K+ channels that are employed in regulatory volume decrease are mediators of the opposing process, i.e. apoptosis.
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Keywords: cation channel; cell volume regulation; epithelial Na+ channel; hypertonic stress; ion selectivity; pharmacology; regulatory volume increase; transient receptor potential

Document Type: Research Article

Affiliations: 1:  Max-Planck-Institut für molekulare Physiologie, Dortmund, Germany 2:  Institut für Molekulare Physiologie und Experimentelle Immunologie, Uni-Klinikum Bonn, Germany 3:  Chirurgische Klinik, Kliniken Dortmund, Germany

Publication date: 2006-05-01

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