Abstract
Distention of cardiac atria promotes atrial fibrillation (AF). Stretch or swelling of myocytes stimulates slow component of IK (IKs) - major repolarizing conductance in the heart. Upregulation of IKs was linked to pathogenesis of AF since gain-of-function mutations in IKs channel genes have been detected in hereditary form of AF. Moreover, stretch of cell membranes changes conformation of AT1 receptor and activates its downstream pathways.
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