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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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pmc free article  (Kaltenbach GmbH)
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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pmc free article  (Hartenstein GmbH)
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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pmc free article  (Tenza Inc)
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Chandler <t>and</t> <t>Meves</t> <t>(1970a,b)</t> reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).
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Chandler and Meves (1970a,b) reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).

Journal: The Journal of Physiology

Article Title: Cardiac action potential repolarization revisited: early repolarization shows all‐or‐none behaviour

doi: 10.1113/JP273651

Figure Lengend Snippet: Chandler and Meves (1970a,b) reported that after internal perfusion of the squid giant axon with NaF, prolonged ‘cardiac‐like’ action potentials were observed (A and B, left). This effect was shown to be due to F3−‐induced slowing of inactivation of a small fraction of the intrinsic squid axon Na+ channels, as illustrated by the simulated ‘action potentials’ (A and B, right). These findings demonstrated the marked influence that a quasi‐steady‐state background inward current can have on action potential waveform. This type of ‘late’ or slowly inactivating Na+ current is now the focus of detailed investigations of the electrophysiological basis for novel anti‐arrhythmic agents. This is because a slowly inactivating or late Na+ current in the human heart that has been identified in a wide variety of pathophysiological settings, and novel antiarrhythmic agents are able to block it selectively (Yang et al. 2015; Belardinelli et al. 2015). This figure is adapted from Chandler and Meves (1970b).

Article Snippet: [ PMC free article ] [ PubMed ] [ Google Scholar ] Chandler WK & Meves H (1970a).

Techniques: Blocking Assay