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PubMed · 16734739

Hypertonicity-induced cation channels.

F Wehner·M Bondarava·F ter Veld·E Endl·H R Nürnberger·T Li
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Abstract

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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AmilorideAnimalsCationsCell MembraneCell Membrane PermeabilityCell SizeEpithelial CellsHumansHypertonic SolutionsOsmolar ConcentrationPotassium ChannelsSodium Channel BlockersJournal ArticleResearch Support, Non-U.S. Gov'tReview

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F Wehner, M Bondarava, F ter Veld, E Endl, H R Nürnberger, T Li. Hypertonicity-induced cation channels.. https://doi.org/10.1111/j.1748-1716.2006.01561.x

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