%0 Journal Article %1 Fabi_1983_C1 %A Fabiato, A. %D 1983 %J Am. J. Physiol. %K 15475522 Adenosine Animals, Caffeine, Calcium, Calmodulin, Cell Compartmentation, Electron, Feedback, Gov't, Guinea Heart Heart, Liver, Male, Microscopy, Myocardium, Non-U.S. P.H.S., Permeability, Phosphorylases, Pigs, Potassium, Ranidae, Research Reticulum, Saponins, Sarcolemma, Sarcoplasmic Sodium, Support, Triphosphate, U.S. Ventricles, %N 1 %P C1--14 %T Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. %V 245 %X The hypothesis of a Ca$^2+$-induced Ca$^2+$ release (CICR) from the sarcoplasmic reticulum (SR) is supported by experiments done in skinned cardiac cells (sarcolemma removed by microdissection). According to this hypothesis, the transsarcolemmal Ca$^2+$ influx does not activate the myofilaments directly but through the induction of a Ca$^2+$ release from the SR. The stimulus gating CICR is not a small change in free Ca$^2+$ concentration (deltafree Ca$^2+$) outside the SR but a function of the rate of this change (deltafree Ca$^2+$/delta t). The initial relatively fast component of the transsarcolemmal Ca$^2+$ current would trigger Ca$^2+$ release; the subsequent slow component, perhaps corresponding to noninactivating Ca$^2+$ channels, would load the SR with an amount of Ca$^2+$ available for release during subsequent beats. Inactivation of CICR is caused by the large increase of free Ca$^2+$ outside the SR resulting from Ca$^2+$ release, which inhibits further release. This negative feedback helps to explain that CICR is not all or none. During relaxation the Ca$^2+$ reaccumulation in the SR is backed up by the Ca$^2+$ efflux across the sarcolemma through Na$^+$-Ca$^2+$ exchange and the sarcolemmal Ca$^2+$ pump. Computations of the Ca$^2+$ buffering in the mammalian ventricular cell and of the systolic transsarcolemmal Ca$^2+$ influx do not support the alternative hypothesis that this influx of Ca$^2+$ is large enough to activate the myofilaments directly. Yet the hypothesis of a CICR can be challenged because of many problems and uncertainties related to the preparations and methods used for skinned cardiac cell experiments.

@article{Fabi_1983_C1, abstract = {The hypothesis of a {C}a$^{2+}$-induced {C}a$^{2+}$ release (CICR) from the sarcoplasmic reticulum (SR) is supported by experiments done in skinned cardiac cells (sarcolemma removed by microdissection). According to this hypothesis, the transsarcolemmal {C}a$^{2+}$ influx does not activate the myofilaments directly but through the induction of a {C}a$^{2+}$ release from the SR. The stimulus gating CICR is not a small change in free {C}a$^{2+}$ concentration (delta[free {C}a$^{2+}$]) outside the SR but a function of the rate of this change (delta[free {C}a$^{2+}$/delta t]). The initial relatively fast component of the transsarcolemmal {C}a$^{2+}$ current would trigger {C}a$^{2+}$ release; the subsequent slow component, perhaps corresponding to noninactivating {C}a$^{2+}$ channels, would load the SR with an amount of {C}a$^{2+}$ available for release during subsequent beats. Inactivation of CICR is caused by the large increase of [free {C}a$^{2+}$] outside the SR resulting from {C}a$^{2+}$ release, which inhibits further release. This negative feedback helps to explain that CICR is not all or none. During relaxation the {C}a$^{2+}$ reaccumulation in the SR is backed up by the {C}a$^{2+}$ efflux across the sarcolemma through {N}a$^{+}$-{C}a$^{2+}$ exchange and the sarcolemmal {C}a$^{2+}$ pump. Computations of the {C}a$^{2+}$ buffering in the mammalian ventricular cell and of the systolic transsarcolemmal {C}a$^{2+}$ influx do not support the alternative hypothesis that this influx of {C}a$^{2+}$ is large enough to activate the myofilaments directly. Yet the hypothesis of a CICR can be challenged because of many problems and uncertainties related to the preparations and methods used for skinned cardiac cell experiments.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Fabiato, A.}, biburl = {https://www.bibsonomy.org/bibtex/282ccfaea7a18bec3564588d1d91551e3/hake}, description = {The whole bibliography file I use.}, file = {Fabi_1983_C1.pdf:Fabi_1983_C1.pdf:PDF}, interhash = {0d648e0d48706a651c05f21d81a567ca}, intrahash = {82ccfaea7a18bec3564588d1d91551e3}, journal = {Am. J. Physiol.}, keywords = {15475522 Adenosine Animals, Caffeine, Calcium, Calmodulin, Cell Compartmentation, Electron, Feedback, Gov't, Guinea Heart Heart, Liver, Male, Microscopy, Myocardium, Non-U.S. P.H.S., Permeability, Phosphorylases, Pigs, Potassium, Ranidae, Research Reticulum, Saponins, Sarcolemma, Sarcoplasmic Sodium, Support, Triphosphate, U.S. Ventricles,}, month = Jul, number = 1, pages = {C1--14}, pmid = {15475522}, timestamp = {2009-06-03T11:21:11.000+0200}, title = {Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum.}, volume = 245, year = 1983 }