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The Strathprints institutional repository is a digital archive of University of Strathclyde research outputs.

Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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Spontaneous and electrically evoked Ca2+ transients in cardiomyocytes of the rat pulmonary vein

Logantha, Sunil Jit R.J. and Cruickshank, Stuart F. and Rowan, Edward G. and Drummond, R.M. (2010) Spontaneous and electrically evoked Ca2+ transients in cardiomyocytes of the rat pulmonary vein. Cell Calcium, 48 (2-3). pp. 150-160. ISSN 0143-4160

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Abstract

The pulmonary vein is surrounded by an external sleeve of cardiomyocytes that are widely recognised to play an important role in atrial fibrillation. While intracellular Ca2+ is thought to influence the electrical activity of cardiomyocytes, there have been relatively few studies examining Ca2+ signalling in these cells. Therefore, using fluo-4 and fluorescence imaging microscopy, we have investigated Ca2+ signalling in an intact section of the rat pulmonary vein. Under resting conditions cardiomyocytes displayed spontaneous Ca2+ transients, which were variable in amplitude and had a frequency of 1.6±0.03 Hz. The Ca2+ transients were asynchronous amongst neighbouring cardiomyocytes and tended to propagate throughout the cell as a wave. Removing extracellular Ca2+ produced a slight reduction in the amplitude and frequency of the spontaneous Ca2+ transients; however, ryanodine (20M) had a much greater effect on the amplitude and reduced the frequency by 94±2%. Blocking IP3 receptors with 2-aminoethoxydiphenyl borate (20M) also reduced the amplitude and frequency (by 73±11%) of these events, indicating the importance of Ca2+ release from the SR. Electrical field stimulation of the pulmonary vein produced Ca2+ transients in cardiomyocytes that were significantly reduced by either voltage-gated Ca2+ channel blockers or ryanodine.