Parasympathetic activation also opens which channels resulting in hyperpolarization?

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Multiple Choice

Parasympathetic activation also opens which channels resulting in hyperpolarization?

Explanation:
Parasympathetic stimulation lowers heart rate by increasing potassium conductance in nodal tissue. Acetylcholine from the vagus binds to M2 muscarinic receptors on pacemaker cells, activating Gi proteins that open G-protein–gated inwardly rectifying K+ channels. The resulting K+ efflux hyperpolarizes the cell, moves the resting potential further from the threshold, and reduces the slope of phase 4 depolarization. This makes it harder for pacemaker cells to reach threshold and slows atrioventricular conduction. Sodium channels opening would depolarize, and L-type calcium channels contribute to depolarization and the plateau rather than hyperpolarization; chloride channels aren't the primary mediators of this parasympathetic effect in the heart.

Parasympathetic stimulation lowers heart rate by increasing potassium conductance in nodal tissue. Acetylcholine from the vagus binds to M2 muscarinic receptors on pacemaker cells, activating Gi proteins that open G-protein–gated inwardly rectifying K+ channels. The resulting K+ efflux hyperpolarizes the cell, moves the resting potential further from the threshold, and reduces the slope of phase 4 depolarization. This makes it harder for pacemaker cells to reach threshold and slows atrioventricular conduction. Sodium channels opening would depolarize, and L-type calcium channels contribute to depolarization and the plateau rather than hyperpolarization; chloride channels aren't the primary mediators of this parasympathetic effect in the heart.

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