Simulations performed on a single cell model of rabbit sinoatrial node activity after prolonged vagal stimulation have been able to reproduce the known characteristics of cycle length recovery, including the presence of rapid and slow recovery phases and the transient undershoot phenomenon known as postvagal tachycardia (PVT). In the model, the PVT component has been hypothesized to result from the recovery of background levels of the muscarinic K+ current iK,ACh from desensitization due to prolonged exposure to acetylcholine (ACh) neurotransmitter. Other components of the recovery were found to be due to the inactivation of iK,ACh after the hydrolysis of ACh (rapid phase) and the recovery of the hyperpolarizing-activated current i(f) from its ACh-induced inhibition (slow phase). The magnitudes of both the rapid component and the PVT were found to increase linearly with preceding vagally mediated increase in cycle length, whereas the gain of the slow component was found to saturate, reflecting the limited contribution of i(f) inhibition to cycle prolongation.
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