Academic Journal
Hypoxia and persistent sodium current
| العنوان: | Hypoxia and persistent sodium current |
|---|---|
| المؤلفون: | Hammarstrom, Anna, Gage, Peter |
| المصدر: | European Biophysics Journal |
| بيانات النشر: | Springer |
| المجموعة: | Australian National University: ANU Digital Collections |
| مصطلحات موضوعية: | Keywords: dithiothreitol, glutathione, ion channel, nitric oxide, sodium calcium exchange protein, sodium channel, sodium channel blocking agent, sodium ion, oxygen, sodium, sodium cyanide, cell damage, channel gating, depolarization, heart arrhythmia, heart muscle Hypoxia, Inactivation, Sodium channels, Sodium current |
| الوصف: | During prolonged depolarization of excitable cells, some voltage-activated, tetrodotoxin-sensitive sodium channels are resistant to inactivation and can continue to open for long periods of time, generating a "persistent" sodium current (INaP). The amplitude of INaP is small [generally less than 1% of the peak amplitude of the transient sodium current (INaT)], activates at potentials close to the resting membrane potential, and is more sensitive to Na channel blocking drugs than INaT. It is thought that persistent Na channels are generated by a change in gating of transient Na channels, possibly because of a change in phosphorylation or protein structure, e.g. loss of the inactivation gate. Drugs that block Na channels can prevent the increase in [Ca2+]i in cardiac cells during hypoxia. Hypoxia increases the amplitude of INaP. Paradoxically, NO causes a similar increase in INaP and the effects of both can be inhibited by reducing agents such as dithiothreitol and reduced glutathione. It is proposed that an increased inflow of Na+ during hypoxia increases [Na+]i, which in turn reverses the Na/Ca exchanger so that [Ca2+]i rises. An increase in INaP and [Ca2+]i could cause arrhythmias and irreversible cell damage. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| تدمد: | 0175-7571 |
| Relation: | http://hdl.handle.net/1885/73198; https://openresearch-repository.anu.edu.au/bitstream/1885/73198/5/MigratedxPub3597_RSD_2002.pdf.jpg; https://openresearch-repository.anu.edu.au/bitstream/1885/73198/7/01_Hammarstrom_Hypoxia_and_persistent_sodium_2002.pdf.jpg |
| DOI: | 10.1007/s00249-002-0218-2 |
| الاتاحة: | http://hdl.handle.net/1885/73198 https://doi.org/10.1007/s00249-002-0218-2 https://openresearch-repository.anu.edu.au/bitstream/1885/73198/5/MigratedxPub3597_RSD_2002.pdf.jpg https://openresearch-repository.anu.edu.au/bitstream/1885/73198/7/01_Hammarstrom_Hypoxia_and_persistent_sodium_2002.pdf.jpg |
| رقم الانضمام: | edsbas.310B9609 |
| قاعدة البيانات: | BASE |
| تدمد: | 01757571 |
|---|---|
| DOI: | 10.1007/s00249-002-0218-2 |