Figure 1. The classical view of cardiomyocyte excitation-contraction coupling and its regulation by β-adrenergic receptors.

Under unstimulated conditions (black arrows), depolarization during an action potential opens LTCCs in T tubules, allowing Ca²⁺ to enter the cell. This trigger Ca²⁺ induces a larger Ca²⁺ release from the SR via RyR2. The increase in Ca²⁺ concentration initiates conformational changes of the myofilaments and thereby contraction. Removal of Ca²⁺ via SERCA and NCX reverses the process. Catecholamines stimulate excitation-contraction coupling (red symbols and lettering) by phosphorylating LTCCs (increased Ca²⁺ influx), PLB (increased Ca²⁺ reuptake into the SR), and myofilament-based troponin I and myosin-binding protein C (increased relaxation). AC, adenylyl cyclise; Gs, stimulatory G protein. Adapted with permission from Nature (35).