Hypertonicity-induced cation channels
| Autor: | E Endl, F ter Veld, Tongju Li, Maryna Bondarava, Frank Wehner, H R Nürnberger |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Cell Membrane Permeability
Potassium Channels Physiology Stereochemistry Sodium Hypertonic Solutions Receptor potential chemistry.chemical_element Amiloride Cell membrane Transient receptor potential channel Sodium channel blocker Cations medicine Animals Humans Cell Size Cell Membrane Osmolar Concentration Epithelial Cells Potassium channel medicine.anatomical_structure chemistry Permeability (electromagnetism) Biophysics Sodium Channel Blockers medicine.drug |
| Zdroj: | Acta Physiologica. 187:21-25 |
| ISSN: | 1748-1716 1748-1708 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|