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Camera-based Measurements of Intracellular [Na+] in Murine Atrial Myocytes
Published on: May 27, 2022
β-Adrenergic modulation of myocardial conduction velocity: Connexins vs. sodium current
Annabel S Campbell1, Scott R Johnstone1, George S Baillie1
1University of Glasgow, United Kingdom.
Insights
Autonomic nervous system influences heart function by altering electrical conduction. This review examines how beta-adrenergic receptor activation impacts ventricular action potential conduction velocity, a key factor in cardiac output.
Area of Science:
- Cardiology
- Electrophysiology
- Autonomic Nervous System
Background:
- The heart's cardiac output is rapidly modulated by the autonomic nervous system, affecting heart rate and contractility.
- While autonomic control of heart rate and contractility is well-studied, its influence on electrical propagation (conduction velocity) is less understood.
- Conduction velocity (CV) of the action potential (AP) is crucial for efficient heart pumping and myocardial electrical stability.
Purpose of the Study:
- To review the literature on the modulation of ventricular AP conduction velocity by beta-adrenergic receptor (β-AR) activation.
- To highlight unresolved issues regarding the mechanisms and extent of β-AR-mediated changes in CV.
Main Methods:
- Review of existing in vivo and in vitro studies on cardiac electrophysiology.
- Analysis of research on cardiomyocyte electrophysiology and gap junction (GJ) function.
- Examination of studies investigating sympathetic nervous system stimulation effects on ventricular CV.
Main Results:
- Sympathetic stimulation shows variable effects on ventricular CV in whole-heart studies, complicated by increased heart rate.
- Cellular studies indicate β-AR activation alters AP shape and amplitude, but its direct impact on CV remains unclear.
- There is limited consensus on how β-AR activation alters GJ conductance and its contribution to CV changes.
Conclusions:
- Understanding the precise mechanisms by which β-AR activation influences ventricular CV is critical.
- Further research is needed to resolve discrepancies regarding GJ conductance modulation and its role in AP propagation.
- Clarifying these mechanisms will enhance our understanding of cardiac electrical stability and pumping efficiency.
Abstract:
The heart is capable of rapid changes in cardiac output: these are caused in large part by changes in the activity of the autonomic nervous system that alter heart rate, force and time course of contraction. While studies of autonomic control have focussed on heart rate and contractile mechanisms, fewer studies have considered the influence of electrical propagation across the chamber. Conduction velocity (CV) of the action potential (AP) is an important variable, which ensures efficient pumping action of the heart and, along with AP duration, is a determinant of the electrical stability of the myocardium. CV depends on multiple factors, including tissue excitability and intercellular resistance: the latter is controlled by the number and arrangement of gap junctions (GJs) linking adjacent cardiac cells. Whole heart studies (in vivo and in vitro) report variable effects of sympathetic nervous system stimulation on ventricular CV, a major complication in interpretation being the accompanying increase in heart rate. At the cellular level, changes in cardiomyocyte electrophysiology, mediated via β-adrenoreceptor (β-AR) activation, alter the AP shape and amplitude but the influence of these effects on the CV is unclear. Alternatively, CV changes may occur via altered GJ conductance, but despite detailed knowledge of the underlying channel protein (connexin), little consensus exists on the extent and time course of the change in GJ conductance induced by AR activation. This review will examine the literature on the modulation of ventricular AP conduction velocity by β-AR activation in a range of physiological preparations and highlight unresolved issues.
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