Pacemaker Function
Pacemaker Function - Related Videos
08:52
Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
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Cited by 13 •
2015
This protocol describes how to produce functional sinus nodal tissue from murine pluripotent stem cells (PSC). T-Box3 (TBX3) overexpression plus cardiac Myosin-heavy-chain (Myh6) promoter antibiotic selection leads to highly pure pacemaker cell aggregates. These “Induced-sinoatrial-bodies” (“iSABs”) contain over 80% pacemaker cells, show highly increased beating rates and are able to pace myocardium ex vivo.
07:38
Isolating and Imaging Live, Intact Pacemaker Regions of Mouse Renal Pelvis by Vibratome Sectioning
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Cited by 1 •
2021
The goal of this protocol is to isolate intact pacemaker regions of the mouse renal pelvis using vibratome sectioning. These sections can then be used for in situ Ca2+ imaging to elucidate Ca2+ transient properties of pacemaker cells and other interstitial cells in vibratome slices.
09:15
fMRI: Functional Magnetic Resonance Imaging
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2023
Functional magnetic resonance imaging (fMRI) is a non-invasive neuroimaging technique used to investigate human brain function and cognition in both healthy individuals and populations with abnormal brain states. Functional MRI utilizes a magnetic resonance signal to detect changes in blood flow that are coupled to neuronal activation when a specific task is performed. This is possible because hemoglobin within the blood has different magnetic properties depending on whether or not it is bound...
02:45
Functional Groups
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2020
Functional groups are a group of atoms with characteristic properties, which when linked to the carbon skeleton of a molecule, alter the properties of that molecule. For example, the presence of certain functional groups on a molecule will make them hydrophilic, whereas others will make them hydrophobic. These functional groups are an indispensable part of organic chemistry and important components of biological molecules, such as carbohydrates, proteins, lipids, and nucleic acids. Each...
09:20
Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Cited by 2 •
2021
This protocol aims to describe a new methodology to measure intrinsic cardiac firing rate using microelectrode array recording of the whole sinoatrial node tissue to identify pacemaking defects in mice. Pharmacological agents can also be introduced in this method to study their effects on intrinsic pacemaking.
FAQs
The funny current, carried through HCN channels, supports the slow diastolic depolarization that occurs between cardiac action potentials. Because this voltage change is gradual rather than abrupt, it helps determine how quickly threshold is reached and therefore influences rhythm timing. Pharmacological changes affecting this current can consequently modify the rate at which pacemaker cells initiate impulses.
Calcium-mediated activity initiates the action potential once gradual depolarization reaches the appropriate level, while potassium-driven repolarization restores the electrical state afterward. These currents therefore influence both impulse initiation and recovery within the pacemaker cycle. Drugs that alter either process may change the timing of successive impulses and contribute to altered heart rate or rhythm.
Autonomic signaling provides a pharmacologically sensitive route for changing pacemaker activity. Agents that modify this signaling can influence the rate at which sinoatrial-node cells progress through their electrical cycle, thereby producing chronotropic effects. This mechanism is important when examining how drugs increase or decrease heart rate without focusing exclusively on direct changes to individual ion channels.
Drug effects may occur at several linked stages: autonomic signaling, ion-channel activity, and cardiac conduction. Altering channel behavior can affect depolarization, calcium-mediated action-potential initiation, or potassium-driven repolarization, whereas changes involving conduction can influence how electrical activity is handled through the heart. Considering these targets helps explain different drug effects on rate and rhythm.
Chronotropic drug studies focus on whether pharmacological treatment changes the timing of impulse generation and, consequently, heart rate. Investigators can interpret those changes in relation to autonomic signaling or ion-channel activity, rather than treating rate alone as the mechanism. This approach connects an observed cardiac response with the electrical process modified by the drug.
Pacemaker activity provides a context for understanding both therapeutic and harmful drug effects on cardiac rhythm. Antiarrhythmic agents may modify impulse generation or conduction, while cardiac toxicity can disrupt these same processes and compromise cardiovascular performance. The framework is also relevant to sinoatrial-node dysfunction, where abnormal impulse generation can impair normal rhythm control.