***************
Invited Symposium: Signal Transduction in Endothelium: Mechano-Sensing, Ion Channels and Intracellular Calcium






Abstract

Calcium: A Multifunctional Messenger In Endothelium

Mechanically Activated Ca2+ -Entry

[Ca2+]i Change

Ion Channels and Driving Force

Conclusion, References & Figures




Discussion
Board

INABIS '98 Home Page Your Session Symposia & Poster Sessions Plenary Sessions Exhibitors' Foyer Personal Itinerary New Search

Ca2+ Signalling in Macrovascular Endothelium: Role of Ion Channels

Nilius, B. (Department of Physiology, KU Leuven, Belgium)
Viana, F. (Department of Physiology, KU Leuven, Belgium)
Kamouchi, M. (Department of Physiology, KU Leuven, Belgium)
Eggermont, J. (Department of Physiology, KU Leuven, Belgium)
Droogmans, G. (Department of Physiology, KU Leuven, Belgium)

Contact Person: Bernd Nilius (bernd.nilius@med.kuleuven.ac.be)


Abstract

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 -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.

Back to the top.
Presentation Number SAnilius0242
Keywords: Ca channels, trp, K channels, hslo, endothelium


| Discussion Board | Next Page | Your Symposium |
Nilius, B.; Viana, F.; Kamouchi, M.; Eggermont, J.; Droogmans, G.; (1998). Ca2+ Signalling in Macrovascular Endothelium: Role of Ion Channels. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/nilius/nilius0242/index.html
© 1998 Author(s) Hold Copyright