Ivabradine augmented the high-frequency dynamic gain of the heart rate response during low- and moderate-intensity vagal nerve stimulation in anesthetized rats under β-blockade.
Does ivabradine alter the heart rate response to vagal nerve stimulation under β-blockade in anesthetized rats?
In a rat model, ivabradine augmented the high-frequency dynamic gain of heart rate response to vagal nerve stimulation under beta-blockade, suggesting an interaction with acetylcholine-sensitive potassium channels.
Since ivabradine (IVA) inhibits hyperpolarization-activated cyclic nucleotide-gated channels, interactions among the sympathetic effect, vagal effect, and IVA can occur in the control of heart rate (HR). To remove the sympathetic effect, we estimated the transfer function from vagal nerve stimulation to HR under β-blockade in anesthetized rats. IVA augmented the high-frequency dynamic gain during low- and moderate-intensity vagal nerve stimulation. Untethering the hyperpolarizing effect of acetylcholine-sensitive potassium channels after IVA may be a possible underlying mechanism.
Kawada et al. (2021) studied this question. Ivabradine was evaluated on Transfer function from vagal nerve stimulation to heart rate (high-frequency dynamic gain). Ivabradine augmented the high-frequency dynamic gain of the heart rate response during low- and moderate-intensity vagal nerve stimulation in anesthetized rats under β-blockade.
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