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Early Ca²+ release S LCS Ca²+ oscillator (SR load dependent) Potential causes: t-tubule loss reduced AP notch B-AR desensitization I SERCA activity RyR desensitization Inward TINCX ca Vmoscillator dv dt Vm Increasing SR load: 1B-AR activation LTCC activity † Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward Incx 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 Icar 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. ß-AR, beta-adrenoreceptor.

Early Ca²+ release S LCS Ca²+ oscillator (SR load dependent) Potential causes: t-tubule loss reduced AP notch B-AR desensitization I SERCA activity RyR desensitization Inward TINCX ca Vmoscillator dv dt Vm Increasing SR load: 1B-AR activation LTCC activity † Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward Incx 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 Icar 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. ß-AR, beta-adrenoreceptor.

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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Early Ca²+ release A 2. A. V Potential causes: t-tubule loss uced AP notch B-AR desensitization SERCA activity RyR desensitization Ca2+ oscillator (SR load dependent) LCS Ica Vmo Inward INCX moscillator dV dt 27 三、 Increasing SR load: 1B-AR activation LTCC activity Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward INCX 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. ß-AR, beta-adrenoreceptor. V
Transcribed Image Text:Early Ca²+ release A 2. A. V Potential causes: t-tubule loss uced AP notch B-AR desensitization SERCA activity RyR desensitization Ca2+ oscillator (SR load dependent) LCS Ica Vmo Inward INCX moscillator dV dt 27 三、 Increasing SR load: 1B-AR activation LTCC activity Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward INCX 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. ß-AR, beta-adrenoreceptor. V
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