Chapter 7 - Electrochemical signaling mechanism in cardiac muscle

Abstract

IRK channels differ from voltage-gated potassium channels since the voltage-gated potassium channels carry outward potassium currents in their operating voltage range and are responsible for repolarizing the exciting cells whereas IRK channels play an important role in setting the resting potential, permitting the plateau phase, inducing rapid final finish of hyperpolarization, and thus preventing the heart from arrhythmias. Using the electrochemical potential of Na+ across the membrane, NCX removes Ca2+ from the cells during the diastole, which likely amplify depolarization through the release of Ca2+ from the SR. The Ca2+ release produces the muscle tone and is considered a basic source of cardiac automaticity. Sympathetic stimulations activate adenylate cyclase to produce cAMP, which makes the HCN channels raise the pulse rate. Through the inactivation of IRK currents, the increase in Ca2+, and the activation of HCN channels, cAMP by stimulation of the sympathetic nerve is implicated in making cardiac muscles to be more excitable. ACh from the vagus nerve binds to the M2 muscarinic receptors (Gi-coupled), which promotes the dissociation of the βγ-complex. Once the IKACh channel protein binding to the βγ-complex causes removal of the plug in the channel, K+ ions flow out of the pacemaker cells causing hyperpolarization, which slows the heart rate.