Muscle contraction RyRs are activated by a calcium trigger, which is brought about by the flow of through the L-type calcium channels. Furthermore, cardiac muscle tend to exhibit diad (or dyad) structures, rather than triads. Excitation-contraction coupling in cardiac muscle cells occurs when an action potential is initiated by pacemaker cells in the sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions. The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes extracellular to enter the cell via L-type calcium channels
Cardiac excitation-contraction coupling In the SAN cAMP binds to an ion channel involved in action potential initiation, speeding up the production of the action potential (see sinoatrial node for more detail). cAMP also, activates a protein called protein kinase A (PKA). PKA affects both the DHPR and RyR, increasing the rise in Ca within the contractile cells and therefore increasing rate of muscle contraction. PKA also affects the myofilaments as well as a protein called phospholamban (PLB; see sarcoplasmic reticulum for more details), speeding up the rate of Cadecline in the cell and so speeding up muscle relaxation. Parasympathetic nerves work by releasing