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Hypertonicity‐induced cation channels
Author(s) -
Wehner F.,
Bondarava M.,
Ter Veld F.,
Endl E.,
Nürnberger H. R.,
Li T.
Publication year - 2006
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2006.01561.x
Subject(s) - amiloride , chemistry , transient receptor potential channel , epithelial sodium channel , trpc , biophysics , ion channel , receptor , pharmacology , sodium , biochemistry , medicine , biology , organic chemistry
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 Gd 3+ and flufenamate) or they are efficiently blocked by Gd 3+ 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.