Ca2+ influx across plasma membranes may trigger Ca2+ release by activating ryanodine-sensitive receptors in the sarcoplasmic reticulum. This process is called Ca2+-induced Ca2+ release, and may be important in regulating cytosolic Ca2+ concentration ([Ca2+]i). In cardiac cells, the initial [Ca2+]i increase, caused by L-type Ca2+ current, is profoundly amplified with Ca2+ release. The synchronized opening of several ryanodine-sensitive Ca2+-releasing channels was detected as discreet and highly localized Ca2+ elevation, and termed as a ‘Ca2+ spark’. A Ca2+ spark is under local control of an L-type Ca2+ channel, and therefore a Ca2+ spark does not normally trigger subsequent Ca2+ sparks in the neighbouring area. In smooth muscle cells, the importance of Ca2+-induced Ca2+ release in elevating [Ca2+]i appears to differ among preparations and species. Significant elevation in [Ca2+]i during depolarization was attributed to Ca2+ release in some smooth muscle cells, but not in others. Ca2+ sparks are also identified in smooth muscle cells, and may play a role as functional elementary events for Ca2+-induced Ca2+ release. At rest, Ca2+ sparks may be also important in regulating smooth muscle membrane potential. Ca2+ sparks occurring at rest do not raise global [Ca2+]i, but trigger spontaneous transient outward currents (STOCs) or spontaneous transient inward currents (STICs), the former producing hyperpolarization; the latter, depolarization. Thus there may be multiple facets for Ca2+-induced Ca2+ release in regulating the contractile status of smooth muscle cells.

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