BBSRC DTA Studentship: Calcium signalling and arrhythmogenesis in pulmonary vein sleeve cells

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Under normal physiological conditions the contraction of each cardiac (heart) muscle cell is under the control of the electrical excitation wave sweeping across the entire heart. The force of contraction of the heart is regulated by the interplay of multiple factors. Our recent interest has been directed towards understanding the modulation of cardiac excitation-contraction (EC) coupling (the signal transduction process) by the protein endothelin-1 (ET-1). It is established that ET-1 can have a significant positive inotropic (increase in contraction) effect in various cardiac tissues from different mammalian species. In addition, it has also been demonstrated that ET-1 can cause arrhythmias (abnormal heart rhythm). The processes underlying the positive inotropic and pro-arrhythmic effects of ET-1 are not entirely clear. Although ET-1 can provide short-term inotropic support for a failing heart, this effect comes with the potential burden of arrhythmogenesis and remodelling. ET-1 concentration has been shown to be increased in cardiac tissues during pathological conditions such as congestive heart failure and myocardial infarction. Understanding the mechanism of action of ET-1 is therefore clinically important.

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