Anatomy & Physiology: The Unity of Form and Function, 7th Edition

Published by McGraw-Hill Education
ISBN 10: 0073403717
ISBN 13: 978-0-07340-371-7

Chapter 19 - Section 19.4 - Electrical and Contractile Activity of the Heart - Before You Go On - Page 728: 16

Answer

The pacemaker potential of the sinoatrial (SA) node in the heart differs from the resting membrane potential of a neuron, and this difference is crucial for creating the heart's rhythmic contractions. **Pacemaker Potential of the SA Node:** The SA node is known as the heart's natural pacemaker because it generates the electrical impulses that initiate each heartbeat. The pacemaker potential of the SA node is characterized by a slow, spontaneous depolarization of its membrane potential over time. Unlike most other cells, including neurons, the SA node cells do not have a stable resting membrane potential. **Resting Membrane Potential of a Neuron:** Neurons typically have a stable resting membrane potential, which is the electrical charge across their cell membrane when they are not actively sending signals. The resting membrane potential of a neuron is relatively constant and is typically around -70 millivolts (mV). **Importance in Creating Heart Rhythm:** The difference in pacemaker potential and resting membrane potential is essential for generating the heart's rhythmic contractions: 1. **Spontaneous Depolarization:** The pacemaker potential of the SA node starts with a slow depolarization from its most negative value (around -60 mV) towards the threshold for generating an action potential (around -40 mV). This slow depolarization is driven by a combination of ion movements, including the **"funny" (If) channels**, which allow sodium and potassium ions to leak into the cell, gradually depolarizing it. 2. **Threshold and Action Potential:** When the pacemaker potential reaches the threshold level, voltage-gated calcium channels open, leading to a rapid influx of calcium ions. This causes the cell to undergo an action potential, resulting in the depolarization phase of the cardiac action potential. 3. **Repolarization and Pacemaker Potential:** After the action potential, the cell undergoes repolarization, primarily due to the efflux of potassium ions. As the membrane potential becomes more negative, the "funny" channels reopen, and the pacemaker potential starts again, initiating the next cycle of depolarization. This cyclic process of slow depolarization, action potential, repolarization, and the subsequent initiation of a new pacemaker potential is what creates the rhythmic contractions of the heart. The unique property of the SA node's pacemaker potential allows it to continuously generate electrical impulses without external input. This intrinsic rhythm-setting ability ensures that the heart beats regularly and initiates the coordinated pumping action necessary for maintaining circulation.

Work Step by Step

The pacemaker potential of the sinoatrial (SA) node in the heart differs from the resting membrane potential of a neuron, and this difference is crucial for creating the heart's rhythmic contractions. **Pacemaker Potential of the SA Node:** The SA node is known as the heart's natural pacemaker because it generates the electrical impulses that initiate each heartbeat. The pacemaker potential of the SA node is characterized by a slow, spontaneous depolarization of its membrane potential over time. Unlike most other cells, including neurons, the SA node cells do not have a stable resting membrane potential. **Resting Membrane Potential of a Neuron:** Neurons typically have a stable resting membrane potential, which is the electrical charge across their cell membrane when they are not actively sending signals. The resting membrane potential of a neuron is relatively constant and is typically around -70 millivolts (mV). **Importance in Creating Heart Rhythm:** The difference in pacemaker potential and resting membrane potential is essential for generating the heart's rhythmic contractions: 1. **Spontaneous Depolarization:** The pacemaker potential of the SA node starts with a slow depolarization from its most negative value (around -60 mV) towards the threshold for generating an action potential (around -40 mV). This slow depolarization is driven by a combination of ion movements, including the **"funny" (If) channels**, which allow sodium and potassium ions to leak into the cell, gradually depolarizing it. 2. **Threshold and Action Potential:** When the pacemaker potential reaches the threshold level, voltage-gated calcium channels open, leading to a rapid influx of calcium ions. This causes the cell to undergo an action potential, resulting in the depolarization phase of the cardiac action potential. 3. **Repolarization and Pacemaker Potential:** After the action potential, the cell undergoes repolarization, primarily due to the efflux of potassium ions. As the membrane potential becomes more negative, the "funny" channels reopen, and the pacemaker potential starts again, initiating the next cycle of depolarization. This cyclic process of slow depolarization, action potential, repolarization, and the subsequent initiation of a new pacemaker potential is what creates the rhythmic contractions of the heart. The unique property of the SA node's pacemaker potential allows it to continuously generate electrical impulses without external input. This intrinsic rhythm-setting ability ensures that the heart beats regularly and initiates the coordinated pumping action necessary for maintaining circulation.
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