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.
|Number of pages||13|
|Journal||Korean Journal of Physiology and Pharmacology|
|Publication status||Published - Jun 2 1998|
All Science Journal Classification (ASJC) codes