Ca2+-induced Ca2+ release in cardiac and smooth muscle cells

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.