Pernicious attrition and inter-RyR2 CICR current control in cardiac muscle.
In cardiac muscle cells, ryanodine receptor (RyR) mediated Ca(2+) release from the sarcoplasmic reticulum (SR) drives the contractile apparatus. Spontaneous bouts of inter-RyR Ca(2+) induced Ca(2+) release (CICR) generate an elemental unit of SR Ca(2+) release called a spark. Sparks are localized events that terminate soon after they begin. The local control of sparks is not clearly understood. In this article, we review the potential regulatory role that the changing single RyR Ca(2+) current may play. Moreover, we aggregate RyR data into a working scheme of inter-RyR CICR current control of sparks and a potential inter-RyR CICR termination mechanism that we call pernicious attrition.
Rush University Medical Center, Department of Molecular Biophysics & Physiology, Section of Cellular Signaling, 1750 West Harrison Street, Chicago, IL 60612, USA.
Dirk
D
Gillespie
Michael
M
Fill
D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D020013:Calcium Signaling; D006801:Humans; D015640:Ion Channel Gating / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism / Q000502:physiology
D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium