Abstract

Calcium: A Multifunctional Messenger In Endothelium

Mechanically Activated Ca²⁺ -Entry

[Ca²⁺]_i Change

Ion Channels and Driving Force

Conclusion, References & Figures

Discussion
Board

Ca2+-signals in endothelial cells (EC) are determined by release from intracellular stores, entry through the plasma membrane, and a variety of Ca2+ sequestration mechanisms. The membrane potential sensitively regulates Ca2+. Nature of Ca2+ entry and its control by the membrane potential are discussed. At least two different types of Ca2+ - entry channels exist: 1. A CRAC-like, highly selective Ca2+ channel which a small current density (0.1pA/pF, 0 mV). No molecular candidate has been identified so far in EC although a differential expression of trp1,3,4 have been detected in endothelial cells. 2. A non-selective cation channel (NSC) which is regulated by agonist-induced Ins(1,4,5)P3 production, requires a permissive intracellular Ca2+-concentrations but is only weakly regulated by intracellular Ca2+ stores. Expression of htrp3 induces functional channels, which resemble NSC. The following ion channels regulate the driving force for Ca2+ entry: an inwardly rectifying K+ channel (Kir2.1), a big-conductance, a Ca2+-activated K+ channel (BKCa; identified as hslo encoded channel) and at least two Cl- channels (a volume regulated anion channel, VRAC, and a Ca2+ activated Cl- channel, CaCC). Some EC only express the a-subunit of hslo. Coexpression of the ß-subunit sensitises BKCa, induces channel-clustering, accentuates agonist-induced hyperpolarization and improves Ca2+ signalling. Blockers of VRAC are efficient to support Ca2+ entry and may provide a new class of tools interfering with NO release.

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Presentation Number SAnilius0242
Keywords: Ca channels, trp, K channels, hslo, endothelium