Effects of components of ischemia on the Kv4.3 current stably expressed in Chinese Hamster Ovary cells

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dc.contributor.author Singarayar, S
dc.contributor.author Singleton, C
dc.contributor.author Tie, H
dc.contributor.author Wyse, K
dc.contributor.author Bursill, J
dc.contributor.author Bauskin, A
dc.contributor.author Wu, W
dc.contributor.author Valenzuela, S
dc.contributor.author Breit, S
dc.contributor.author Campbell, T
dc.date.accessioned 2010-05-28T09:49:27Z
dc.date.issued 2002-02-01
dc.identifier.citation Journal of Molecular and Cellular Cardiology, 2002, 34 (2), pp. 197 - 207
dc.identifier.issn 0022-2828
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/9414
dc.description.abstract We investigated the effects of three components of ischemia: external acidosis (pH = 6.0), extracellular hyperkalemia ([K+] = 20 mmol/l), and resting membrane depolarization to -60 mV. on Kv4.3 current stably expressed in Chinese Hamster Ovary cells. We used single electrode whole cell patch clamp techniques to study changes in the current elicited. External acidosis caused a positive shift in the steady state activation curve from -13.4±2.1 mV to -3.3±1.5 mV (n = 8, P = 0.004) and the steady state inactivation curve from -56.5±0.4 mV to -46.7±0.5 mV (n = 14, P<0.0001). Acidosis also caused an acceleration of recovery from inactivation with the t1/2 decreasing from 306 ms (95% CI 287-327 ms) to 194 ms (95% CI 182-207 ms), (n = 14, P<0.05). Hyperkalemia did not affect any of these parameters. Combined acidosis and hyperkalemia produced effects similar to those seen with acidosis. Changing the holding potential from -90 mV to -60 mV with test potentials of +5 and +85 mV decreased the peak currents by 34.1% and 32.4% respectively (n = 14). However, in the presence of external acidosis the decrease in peak currents induced by changing the holding potential was less marked. In acidotic bath the peak current at -60 mV was reduced by only 13.6% at a test potential of +5 mV and 12.3% at a test potential of +85 mV (n = 14). Taken together our data suggest that the membrane depolarization and changes in pH which occur under ischemic conditions would be accompanied by relative preservation of Kv4.3 currents and provide a molecular basis for the observation of preserved epicardial Ito and epicardial action potential duration (APD) shortening in ischemia. © 2002 Elsevier Science Ltd.
dc.language eng
dc.relation.isbasedon 10.1006/jmcc.2001.1502
dc.title Effects of components of ischemia on the Kv4.3 current stably expressed in Chinese Hamster Ovary cells
dc.type Journal Article
dc.parent Journal of Molecular and Cellular Cardiology
dc.journal.volume 2
dc.journal.volume 34
dc.journal.number 2 en_US
dc.publocation USA en_US
dc.identifier.startpage 197 en_US
dc.identifier.endpage 207 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 0304 Medicinal and Biomolecular Chemistry
dc.for 0306 Physical Chemistry (Incl. Structural)
dc.for 1004 Medical Biotechnology
dc.personcode 010690
dc.percentage 50 en_US
dc.classification.name Medical Biotechnology en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords Acidosis
dc.description.keywords Hyperkalemia
dc.description.keywords Ischemia
dc.description.keywords Kv4.3
dc.description.keywords Transient outward current
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Strength - Health Technologies
utslib.copyright.status Closed Access
utslib.copyright.date 2015-04-15 12:17:09.805752+10
pubs.consider-herdc false


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