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Abstract
Nuclear calcium (Ca2+) signalling play a major role in cardiac excitation-transcription coupling. The origin of nuclear Ca2+ transient is still controversial. It has been suggested that Ca2+ diffusion from the cytosol through the nuclear pores or perinuclear and intranuclear Ca2+ release mechanisms, mostly via the inositol-3-phosphate receptors (IP3R), participate to nuclear Ca2+ transient. In rabbits subjected to rapid atrial pacing (RAP, 600bp, 5 days), a model for atrial fibrillation (AF), we recently observed that central-cellular, but not subsarcolemmal Ca2+ transient, was largely reduced.
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