Ca²⁺ signalling in endothelial cells: Role of ion channels

Ca²⁺-signals in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of Ca²⁺ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for Ca²⁺ entry: an inwardly rectifying K⁺ channel, identified as Kir2.1, a big-conductance, Ca²⁺-activated K⁺ channel (hslo) and at least two Cl^- channels (a volume regulated Cl^-channel, VRAC, and a Ca²⁺ activated Cl^- channel, CaCC). At least two different types of Ca²⁺-entry channels exist: 1. A typical CRAC-like, highly selective Ca²⁺ channel is described. Current density for this Ca²⁺ entry is approximately 0.1pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for Ca²⁺ entry is a more non-selective channel, which might be regulated by intracellular Ca²⁺. Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non- selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of Ca²⁺- oscillations in endothelial cells is also presented.