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10.1016/j.yjmcc.2016.01.024 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2016.01.024 C4807626!4807626!26827896     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Mol+Cell+Cardiol 2016 ; 92 (ä): 82-92 Nephropedia Template TP {{tp|p=26827896|t=2016. Ryanodine receptor sensitivity governs the stability and synchrony of local calcium release during cardiac excitation-contraction coupling |pdf=|usr=}}{{26827896}} gab.com Text Ryanodine receptor sensitivity governs the stability and synchrony of local calcium release during cardiac excitation-contraction coupling JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26827896 #FOAvip Calcium-induced calcium release is the principal mechanism that triggers the cell-wide [Ca2+]i transient that activates muscle contraction during cardiac excitation-contraction coupling (ECC). Here, we characterize this process in mouse cardiac myocytes with a novel mathematical action potential (AP) model that incorporates realistic stochastic gating of voltage-dependent L-type calcium (Ca2+) channels (LCCs) and sarcoplasmic reticulum (SR) Ca2+ release channels (the ryanodine receptors, RyR2s). Depolarization of the sarcolemma during an AP stochastically activates the LCCs elevating subspace [Ca2+] within each of the cell?s 20,000 independent calcium release units (CRUs) to trigger local RyR2 opening and initiate Ca2+ sparks, the fundamental unit of triggered Ca2+ release. Synchronization of Ca2+ sparks during systole depends on the nearly uniform cellular activation of LCCs and the likelihood of local LCC openings triggering local Ca2+ sparks (ECC fidelity). The detailed design and true SR Ca2+ pump/leak balance displayed by our model permits investigation of ECC fidelity and Ca2+ spark fi-delity, the balance between visible (Ca2+ spark) and invisible (Ca2+ quark/sub-spark) SR Ca2+ release events. Excess SR Ca2+ leak is examined as a disease mechanism in the context of ?catecholaminergic polymorphic ventricular tachycardia (CPVT)?, a Ca2+-dependent arrhythmia. We find that that RyR2s (and therefore Ca2+ sparks) are relatively insensitive to LCC openings across a wide range of membrane potentials; and that key differences exist between Ca2+ sparks evoked during quiescence, diastole, and systole. The enhanced RyR2 [Ca2+]i sensitivity during CPVT leads to increased Ca2+ spark fidelity resulting in asynchronous systolic Ca2+ spark activity. It also produces increased diastolic SR Ca2+ leak with some prolonged Ca2+ sparks that at times become ?metastable? and fail to efficiently terminate. There is a huge margin of safety for stable Ca2+ handling within the cell and this novel mechanistic model provides insight into the molecular signaling characteristics that help maintain overall Ca2+ stability even under the conditions of high SR Ca2+ leak during CPVT. Finally, this model should provide tools for investigators to examine normal and pathological Ca2+ signaling characteristics in the heart. Twit Text FOAVip Ryanodine receptor sensitivity governs the stability and synchrony of local calcium release during cardiac excitation-contraction coupling ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26827896 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26827896 #FOAvip English Wikipedia <ref>{{Cite pmid|26827896}}</ref> Ryanodine receptor sensitivity governs the stability and synchrony of local calcium release during cardiac excitation-contraction coupling #MMPMID26827896 Wescott AP; Jafri MS; Lederer W; Williams GS J Mol Cell Cardiol 2016[Mar]; 92 (ä): 82-92 PMID26827896show ga Calcium-induced calcium release is the principal mechanism that triggers the cell-wide [Ca2+]i transient that activates muscle contraction during cardiac excitation-contraction coupling (ECC). Here, we characterize this process in mouse cardiac myocytes with a novel mathematical action potential (AP) model that incorporates realistic stochastic gating of voltage-dependent L-type calcium (Ca2+) channels (LCCs) and sarcoplasmic reticulum (SR) Ca2+ release channels (the ryanodine receptors, RyR2s). Depolarization of the sarcolemma during an AP stochastically activates the LCCs elevating subspace [Ca2+] within each of the cell?s 20,000 independent calcium release units (CRUs) to trigger local RyR2 opening and initiate Ca2+ sparks, the fundamental unit of triggered Ca2+ release. Synchronization of Ca2+ sparks during systole depends on the nearly uniform cellular activation of LCCs and the likelihood of local LCC openings triggering local Ca2+ sparks (ECC fidelity). The detailed design and true SR Ca2+ pump/leak balance displayed by our model permits investigation of ECC fidelity and Ca2+ spark fi-delity, the balance between visible (Ca2+ spark) and invisible (Ca2+ quark/sub-spark) SR Ca2+ release events. Excess SR Ca2+ leak is examined as a disease mechanism in the context of ?catecholaminergic polymorphic ventricular tachycardia (CPVT)?, a Ca2+-dependent arrhythmia. We find that that RyR2s (and therefore Ca2+ sparks) are relatively insensitive to LCC openings across a wide range of membrane potentials; and that key differences exist between Ca2+ sparks evoked during quiescence, diastole, and systole. The enhanced RyR2 [Ca2+]i sensitivity during CPVT leads to increased Ca2+ spark fidelity resulting in asynchronous systolic Ca2+ spark activity. It also produces increased diastolic SR Ca2+ leak with some prolonged Ca2+ sparks that at times become ?metastable? and fail to efficiently terminate. There is a huge margin of safety for stable Ca2+ handling within the cell and this novel mechanistic model provides insight into the molecular signaling characteristics that help maintain overall Ca2+ stability even under the conditions of high SR Ca2+ leak during CPVT. Finally, this model should provide tools for investigators to examine normal and pathological Ca2+ signaling characteristics in the heart. äRyanodine receptor sensitivity governs the stability and synchrony of (epmc).pdf DeepDyve Pubget Overpricing