Ca2+ signalling in endothelial cells: Role of ion channels.
- Author:
Bernd NILIUS
1
;
Felix VIANA
;
Masahiro KAMOUCHI
;
Cristina FASOLATO
;
Jan EGGERMONT
;
Guy DROOGMANS
Author Information
1. KU Leuven, Campus Gasthuisberg, Department of Physiology, B-3000 LEUVEN, Belgium.
- Publication Type:Original Article
- Keywords:
Endothelium;
Ca2+-entry channels;
potassium channels;
Ca2+-oscillations
- MeSH:
Cell Membrane;
Endothelial Cells*;
Endothelium;
Ion Channels*;
Mast Cells;
Potassium Channels;
Pulmonary Artery
- From:The Korean Journal of Physiology and Pharmacology
1998;2(2):133-145
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
