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https://hdl.handle.net/2440/11937
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dc.contributor.author | Ju, Y.K. | - |
dc.contributor.author | Saint, D. | - |
dc.contributor.author | Gage, P. | - |
dc.date.issued | 1996 | - |
dc.identifier.citation | The Journal of Physiology, 1996; 497(2):337-347 | - |
dc.identifier.issn | 0022-3751 | - |
dc.identifier.issn | 1469-7793 | - |
dc.identifier.uri | http://hdl.handle.net/2440/11937 | - |
dc.description.abstract | 1. A persistent inward current activated by depolarization was recorded using the whole-cell, tight seal technique in rat isolated cardiac myocytes. The amplitude of the inward current increased when cells were exposed to a solution with low oxygen tension. 2. The persistent inward current had the characteristics of the persistent Na+ current described previously in rat ventricular myocytes: it was activated at negative potentials (-70 mV), reversed close to the equilibrium potential for Na+ (ENa), was blocked by TTX and was resistant to inactivation. 3. Persistent single Na+ channel currents activated by long (200-400 ms) depolarizations were recorded in cell-attached patches on isolated ventricular myocytes. Hypoxia increased the frequency of opening of the persistent Na+ channels. 4. Persistent Na+ channels recorded during hypoxia had characteristics similar to those of persistent Na+ channels recorded at normal oxygen tensions. They had a null potential at ENa, their amplitude varied with [Na+], they were resistant to inactivation and their mean open time increased with increasing depolarization. 5. The persistent Na+ channels in cell-attached patches were blocked by TTX (50 microM) in the patch pipette and by lidocaine (100 microM). 6. It was concluded that hypoxia increases the open probability of TTX-sensitive, inactivation-resistant Na+ channels. The voltage dependence of these channels, and their greatly increased activity during hypoxia, suggest that they may play an important role in the generation of arrhythmias during hypoxia. | - |
dc.description.statementofresponsibility | Y.-K. Ju, D. A. Saint, and P. W. Gage | - |
dc.language.iso | en | - |
dc.publisher | The Physiological Society | - |
dc.source.uri | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1160988/ | - |
dc.subject | Myocardium | - |
dc.subject | Heart Ventricles | - |
dc.subject | Animals | - |
dc.subject | Rats | - |
dc.subject | Rats, Wistar | - |
dc.subject | Sodium | - |
dc.subject | Lidocaine | - |
dc.subject | Tetrodotoxin | - |
dc.subject | Sodium Channels | - |
dc.subject | Anti-Arrhythmia Agents | - |
dc.subject | Electrophysiology | - |
dc.subject | Ion Channel Gating | - |
dc.subject | Membrane Potentials | - |
dc.subject | Time Factors | - |
dc.subject | Hypoxia | - |
dc.title | Hypoxia increases persistent sodium current in rat ventricular myocytes | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1113/jphysiol.1996.sp021772 | - |
pubs.publication-status | Published | - |
Appears in Collections: | Aurora harvest 2 Physiology publications |
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