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The Strathprints institutional repository is a digital archive of University of Strathclyde research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including those from the School of Psychological Sciences & Health - but also papers by researchers based within the Faculties of Science, Engineering, Humanities & Social Sciences, and from the Strathclyde Business School.

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Measurement and modelling of Ca2+ waves in isolated rabbit ventricular cardiomyocytes

MacQuaide, N. and Dempster, J. and Smith, G.L. (2007) Measurement and modelling of Ca2+ waves in isolated rabbit ventricular cardiomyocytes. Biophysical Journal, 93 (7). pp. 2581-2595. ISSN 0006-3495

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The time course and magnitude of the Ca2+ fluxes underlying spontaneous Ca2+ waves in single permeabilized ventricular cardiomyocytes were derived from confocal Fluo-5F fluorescence signals. Peak flux rates via the sarcoplasmic reticulum (SR) release channel (RyR2) and the SR Ca2+ ATPase (SERCA) were not constant across a range of cellular [Ca2+] values. The Ca2+ affinity (Kmf) and maximum turnover rate (Vmax) of SERCA and the peak permeability of the RyR2-mediated Ca2+ release pathway increased at higher cellular [Ca2+] loads. This information was used to create a computational model of the Ca2+ wave, which predicted the time course and frequency dependence of Ca2+ waves over a range of cellular Ca2+ loads. Incubation of cardiomyocytes with the Ca2+ calmodulin (CaM) kinase inhibitor autocamtide-2-related inhibitory peptide (300 nM, 30 mins) significantly reduced the frequency of the Ca2+ waves at high Ca2+ loads. Analysis of the Ca2+ fluxes suggests that inhibition of CaM kinase prevented the increases in SERCA Vmax and peak RyR2 release flux observed at high cellular [Ca2+]. These data support the view that modification of activity of SERCA and RyR2 via a CaM kinase sensitive process occurs at higher cellular Ca2+ loads to increase the maximum frequency of spontaneous Ca2+ waves.