Fig. 5. Flow diagram for two interacting positive-feedback mechanisms that can drive Vm and Ca2+ oscillations during EADs. The red inner cycle represents the well-established Vm oscillator, wherein an increase in dv/dt (caused by a relative increase in depolarizing currents compared to repola- rizing currents, e.g., text in orange box at Lower Right) leads to voltage- dependent reactivation of Ica which in turn causes further depolarization. The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator mechanism for EAD initiation. Reduced early Ca²+ release and/or increased SR load increases LCS production, and the resulting increase in inward INCX tends to depolarize the membrane which then feeds onto Ica to trigger additional LCS. Green arrows indicate possible factors contributing to EAD initiation. B-AR, beta-adrenoreceptor.

Introductory Circuit Analysis (13th Edition)
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ISBN:9780133923605
Author:Robert L. Boylestad
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Chapter1: Introduction
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Use the information in this diagram to make your original simpler diagram.
Early Ca²+
release
Potential causes:
t-tubule loss
reduced AP notch
B-AR desensitization
SERCA activity
RyR desensitization
Ca²+ oscillator
(SR load dependent)
LCS
Inward
INCX
Ica Vm oscillator dv
dt
Increasing SR load:
16-AR activation
LTCC activity
Stimulus rate
↑intracellular Na
Repol.
reserve
Potential causes:
K* current density
Late Nat currents
Ice reactivation
Inward luck
Fig. 5. Flow diagram for two interacting positive-feedback mechanisms
that can drive Vm and Ca²+ oscillations during EADs. The red inner cycle
represents the well-established Vm oscillator, wherein an increase in dv/dt
(caused by a relative increase in depolarizing currents compared to repola-
rizing currents, e.g., text in orange box at Lower Right) leads to voltage-
dependent reactivation of Ica which in turn causes further depolarization.
The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator
mechanism for EAD initiation. Reduced early Ca²+ release and/or increased
SR load increases LCS production, and the resulting increase in inward INCX
tends to depolarize the membrane which then feeds onto Ica to trigger
additional LCS. Green arrows indicate possible factors contributing to
EAD initiation. P-AR, beta-adrenoreceptor.
Transcribed Image Text:Early Ca²+ release Potential causes: t-tubule loss reduced AP notch B-AR desensitization SERCA activity RyR desensitization Ca²+ oscillator (SR load dependent) LCS Inward INCX Ica Vm oscillator dv dt Increasing SR load: 16-AR activation LTCC activity Stimulus rate ↑intracellular Na Repol. reserve Potential causes: K* current density Late Nat currents Ice reactivation Inward luck Fig. 5. Flow diagram for two interacting positive-feedback mechanisms that can drive Vm and Ca²+ oscillations during EADs. The red inner cycle represents the well-established Vm oscillator, wherein an increase in dv/dt (caused by a relative increase in depolarizing currents compared to repola- rizing currents, e.g., text in orange box at Lower Right) leads to voltage- dependent reactivation of Ica which in turn causes further depolarization. The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator mechanism for EAD initiation. Reduced early Ca²+ release and/or increased SR load increases LCS production, and the resulting increase in inward INCX tends to depolarize the membrane which then feeds onto Ica to trigger additional LCS. Green arrows indicate possible factors contributing to EAD initiation. P-AR, beta-adrenoreceptor.
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