Vagal (parasympathetic) activation affects pacemaker cells by which change in threshold and AP duration?

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Multiple Choice

Vagal (parasympathetic) activation affects pacemaker cells by which change in threshold and AP duration?

Explanation:
Vagal (parasympathetic) input to pacemaker cells increases outward potassium current, which hyperpolarizes the cell and slows the pace of spontaneous diastolic depolarization (the phase 4 slope). With the membrane resting at a more negative level, the distance to the threshold for triggering a new action potential becomes larger, so it takes longer to reach threshold. That makes the time to threshold increase. At the same time, the autonomic influence also modulates currents that shape the nodal action potential, including reducing inward calcium current and altering repolarizing potassium currents. This combined effect tends to slow the progression of the cycle and can lengthen the overall duration of the nodal action potential. So both the time to reach threshold and the duration of the action potential are increased with vagal activation.

Vagal (parasympathetic) input to pacemaker cells increases outward potassium current, which hyperpolarizes the cell and slows the pace of spontaneous diastolic depolarization (the phase 4 slope). With the membrane resting at a more negative level, the distance to the threshold for triggering a new action potential becomes larger, so it takes longer to reach threshold. That makes the time to threshold increase.

At the same time, the autonomic influence also modulates currents that shape the nodal action potential, including reducing inward calcium current and altering repolarizing potassium currents. This combined effect tends to slow the progression of the cycle and can lengthen the overall duration of the nodal action potential. So both the time to reach threshold and the duration of the action potential are increased with vagal activation.

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