作者: LONG-SHENG SONG , SILVIA GUATIMOSIM , LETICIA GÓMEZ-VIQUEZ , ERIC A. SOBIE , ANDREW ZIMAN
关键词: Calcium signaling 、 Depolarization 、 Endocrinology 、 Biophysics 、 Patch clamp 、 Myocyte 、 Calcium 、 Internal medicine 、 Biology 、 Ryanodine receptor 、 Dihydropyridine 、 Cardiac action potential
摘要: Ca(2+) sparks in heart muscle are activated on depolarization by the influx of through dihydropyridine receptors sarcolemmal (SL) and transverse tubule (TT) membranes. The cardiac action potential is thus able to synchronize [Ca(2+)](i) transient as release throughout cell. Increases amount within sarcoplasmic reticulum (SR) underlie augmented globally an increase sensitivity ryanodine (RyRs) be triggered local [Ca(2+)](i). In a similar manner, phosphorylation RyRs protein kinase A (PKA) increases Heart failure other diseases associated with changes SR content, state RyRs, signaling defects arrhythmias. Additional tubules nearby junctional may contribute alterations signaling. Here we briefly discuss how TT organization can influence triggering excitation-contraction (EC) coupling. High speed imaging methods used combination single cell patch clamp experiments investigate abnormal regulated health disease. Three issues examined this presentation: (1) normal Ca(2+)-induced sparks, (2) disease, (3) propagation waves elevated