LAUSR

Each heart beat in every cardiac myocyte begins with the surface membrane depolarization during an action potential that opens L-type Ca2+ channels and allows the influx of a small amount of extracellular Ca2+ that triggers a larger release of Ca2+ from the intracellular store, the sarcoplasmic reticulum (SR), through ryanodine receptors (RyR2).1,2 This process, known as Ca2+-induced Ca2+-release, is the primary mechanism underlying excitation–contraction coupling in the heart. Cardiac myocytes are relatively large cells, and efficient cardiac function requires not only the rapid sequential activation of contraction between cells but also the simultaneous activation of the contractile apparatus within each cell. To accomplish this, adult cardiac myocytes localize L-type Ca2+ channels in deep membrane invaginations known as transverse tubules (T-tubules), located along the Z-lines adjacent to the SR Ca2+ release channels in highly ordered structures known as dyads. The potential importance of these organized junctional membrane complexes has been defined during the last decade using in situ imaging techniques that show their loss in pathological conditions, including myocardial infarction and heart failure.3 Article, see p 110 …