Abstract
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.