Calcium signalling in endothelial cells

Cardiovasc Res. 2000 Oct;48(1):13-22. doi: 10.1016/s0008-6363(00)00172-3.

Abstract

Vascular endothelial cells are ubiquitous for their presence in each and every vessel and unique for their multifunctional nature. A large number of endothelial functions depend to various extents on changes in intracellular Ca(2+) concentration. Reviewed are endothelial Ca(2+) stores, Ca(2+) channels, and in-out-in Ca(2+) signalling events, from ligand-binding on the plasma membrane into depletion of intracellular Ca(2+) stores and therefrom out to transplasmalemmal Ca(2+) entry that is of prime importance for many endothelial functions. Special emphasis is placed on mechanisms regulating store-operated Ca(2+) entry including a Ca(2+) influx factor, the vesicle secretion-like model, the conformational coupling model, the membrane potential, cytochrome P450, protein tyrosine kinase, myosin light chain kinase and nitric oxide.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium / metabolism
  • Calcium Channels / metabolism*
  • Calcium Signaling / physiology*
  • Cell Membrane / metabolism
  • Cytochrome P-450 Enzyme System / metabolism
  • Endoplasmic Reticulum / metabolism
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / metabolism*
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Membrane Potentials
  • Mitochondria / metabolism
  • Models, Cardiovascular*
  • Myosin-Light-Chain Kinase / metabolism
  • Nitric Oxide / metabolism
  • Protein-Tyrosine Kinases / metabolism

Substances

  • Calcium Channels
  • Nitric Oxide
  • Inositol 1,4,5-Trisphosphate
  • Cytochrome P-450 Enzyme System
  • Protein-Tyrosine Kinases
  • Myosin-Light-Chain Kinase
  • Calcium