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dc.contributor.authorHussain, Munir*
dc.contributor.authorChorvatova, A.*
dc.date.accessioned2009-07-14T09:31:23Z
dc.date.available2009-07-14T09:31:23Z
dc.date.issued2009-07-14
dc.identifier.citationHussain, M., Chorvatova, A. (2003). Effects of caffeine on potassium currents in isolated rat ventricular myocytes. Pflugers Archiv European Journal of Physiology. Vol. 446, No. 4, pp. 422-428.
dc.identifier.urihttp://hdl.handle.net/10454/3003
dc.descriptionNo
dc.description.abstractRapid exposure of cardiac muscle to high concentrations of caffeine releases Ca 2+ from the sarcoplasmic reticulum (SR). This Ca 2+ is then extruded from the cell by the Na +/Ca 2+ exchanger. Measurement of the current carried by the exchanger ( I Na/Ca) can therefore be used to estimate of the Ca 2+ content of the SR. Previous studies have shown that caffeine, however, can also inhibit K + currents. We therefore investigated whether the inhibitory effects of caffeine on these currents could contaminate measurements of I Na/Ca. Caffeine caused partial inhibition of the inward rectifier K + current ( I K1): the outward current at ¿40 mV was 1.15±0.24 pA/pF in control and decreased to 0.34±0.15 pA/pF in the presence of 10 mmol/l caffeine ( P<0.05, n=15). This was similar to the effect of caffeine on the holding current observed at ¿40 mV in the absence of K + channel block and could therefore account for the contaminating effects of caffeine observed during measurements of I Na/Ca. Moreover, caffeine also partially inhibited the transient outward ( I to) and the delayed rectifier ( I K) K + currents.
dc.language.isoen
dc.subjectCaffeine
dc.subjectPotassium Currents
dc.subjectRat Ventricular
dc.subjectMyocytes
dc.subjectCardiac Muscle
dc.subjectCalcium Ion
dc.subjectSodium/Potassium exchanger
dc.titleEffects of caffeine on potassium currents in isolated rat ventricular myocytes
dc.status.refereedYes
dc.typeArticle
dc.type.versionNo full-text in the repository
dc.identifier.doihttps://doi.org/10.1007/s00424-003-1031-1
dc.openaccess.statusclosedAccess


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