Korean J Physiol Pharmacol.
1998 Apr;2(2):133-145.
Ca2+ signalling in endothelial cells: Role of ion channels
- Affiliations
-
- 1KU Leuven, Campus Gasthuisberg, Department of Physiology, B-3000 LEUVEN, Belgium.
Abstract
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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 0.1 pA/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.