Abstract
Rationale In type I diabetes mellitus (T1DM) there is increased risk of bradyarrhythmias as a result of dysfunction of the sinoatrial-node/the primary pacemaker of the heart. We showed that streptozocin (STZ)- induced T1DM rats had decreased in-vivo heart rate (1). The aim of this study was to investigate the cellular basis of T1DM on the sinoatrial-node using the STZ rat model. Methods Diabetes was induced with STZ in male Wistar rats as previously described (1). Extracellular potential and whole cell patch clamp recordings were used. Protein expression was investigated using immunohistochemistry. The research was conducted in accordance with the Guide for the Care and Use for Laboratory Animals in UAE and UK. Results Compared to controls, diabetic rats showed higher heart-to-body weight ratio (16%) and blood glucose (428%) (n = 32, P Conclusion Complex interplay between membrane currents and Ca2+-clock signalling may increase risk of bradyarrhythmia.
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