Non-capacitative calcium entry--extension of the possibilities for calcium entry in vascular tissue.

The functional state of blood vessels is regulated by the calcium sensitivity of the contractile elements and the intracellular calcium concentration. The latter is determined by the balance between the activity of calcium sources (influx from the extracellular space and release from intracellular stores), the activity of calcium sinks (extrusion to the extracellular space and sequestration into intracellular stores), and the capacity of calcium buffers. Contractile reactions of blood vessels are depressed considerably after removal of extracellular calcium ions, emphasizing the importance of calcium entry for vessel contractility. Classically, voltage-operated calcium influx via L-type calcium channels had been assigned a leading role in calcium entry. However, a considerable number of contractile reactions have been shown to be resistant or only partly affected by specific inhibitors of voltage-operated calcium channels. Thus, voltage-independent calcium entry must contribute to vessel contractility. Indeed, several such mechanisms have been identified in different cell types [1–3], including smooth muscle [4]: 1) receptor-operated calcium entry, activated by direct binding of an external ligand to the channel; 2) storeoperated or capacitative calcium entry (CCE), activated by calcium release from intracellular stores or, more precisely, by the degree of store depletion; 3) non-store-operated or non-capacitative calcium entry (non-CCE), activated independently of store depletion. In the past, the latter was often termed receptor-operated calcium entry. However, in view of the fact that all calcium entry mechanisms can be activated by agonist-receptor interaction, this term does not have much