Wolff–Parkinson–White syndrome cardiac action potential arises in the sinoatrial (SA) node, which is located in the right atrium. From there, the electrical stimulus is transmitted via internodal pathways to the atrioventricular (AV) node. After a brief delay at the AV node, the stimulus travels through the bundle of His to the left and right bundle branches and then to the Purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular myocardium. The AV node serves an important function as a "gatekeeper", limiting the electrical activity that reaches the ventricles. In situations where the atria generate excessively
Sinoatrial node (in particular T1-T4). These nerves release a neurotransmitter called noradrenaline (NA). This binds to a receptor on the SA node membrane, called a beta-1adrenoceptor. Binding of NA to this receptor activates a G-protein (in particular a G-Protein, S for stimulatory) which initiates a series of reactions (known as the cAMP pathway) that results in the production of a molecule called cyclic adenosinemonophosphate (cAMP). This cAMP binds to the HCN channel (see above). Binding of cAMP to the HCN, increases the flow of Na and K into the cell, speeding up the pacemaker potential, so producing action potentials at a quicker