Final answer:
The increase in ventricular contractility is mediated through a second-messenger pathway involving the activation of β-adrenergic receptors, production of cAMP, activation of protein kinase A (PKA), and modulation of calcium ion handling within the cardiomyocytes, enhancing the force of contraction.
Step-by-step explanation:
The increase in ventricular contractility is partly achieved through a second-messenger pathway initiated by the binding of hormones like adrenaline to β-adrenergic receptors on the heart muscle cell surface. This binding activates a G protein, which in turn activates adenylate cyclase, leading to an increase in cyclic AMP (cAMP) within the cell. The elevated levels of cAMP activate protein kinase A (PKA), which phosphorylates various target proteins, leading to an increase in calcium entry into the cell during the plateau phase of the action potential. This mechanism allows more calcium to be available to the sarcomeres, resulting in enhanced contractile activity or positive inotropy. Additionally, PKA modulates the sarcoplasmic reticulum's calcium uptake and release, further contributing to the contractility of the cardiac muscle.
Moreover, PKA also phosphorylates and inhibits the function of the myosin binding protein C, which when phosphorylated decreases its inhibition on actin and myosin interactions, further enhancing contractile force. PKA may also phosphorylate phospholamban, a protein that inhibits the sarcoplasmic reticulum Ca2+-ATPase (SERCA), thereby increasing the reuptake of calcium into the sarcoplasmic reticulum for the next contraction.
The electrical events in the heart such as the wave of depolarization initiate the contraction process, and the second-messenger pathways modify it to adjust the force and efficiency of the heart's pumping according to the body's needs.