Accessibility navigation


Hypoxic modulation of ca(2+) signaling in human venous and arterial endothelial cells

Aley, P. K., Bauer, C. C., Dallas, M. L., Boyle, J. P., Porter, K. E. and Peers, C. (2009) Hypoxic modulation of ca(2+) signaling in human venous and arterial endothelial cells. The Journal of Membrane Biology, 227 (3). pp. 151-158. ISSN 1432-1424

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1007/s00232-008-9147-z

Abstract/Summary

Our understanding of vascular endothelial cell physiology is based on studies of endothelial cells cultured from various vascular beds of different species for varying periods of time. Systematic analysis of the properties of endothelial cells from different parts of the vasculature is lacking. Here, we compare Ca(2+) homeostasis in primary cultures of endothelial cells from human internal mammary artery and saphenous vein and how this is modified by hypoxia, an inevitable consequence of bypass grafting (2.5% O(2), 24 h). Basal [Ca(2+)]( i ) and store depletion-mediated Ca(2+) entry were significantly different between the two cell types, yet agonist (ATP)-mediated mobilization from endoplasmic reticulum stores was similar. Hypoxia potentiated agonist-evoked responses in arterial, but not venous, cells but augmented store depletion-mediated Ca(2+) entry only in venous cells. Clearly, Ca(2+) signaling and its remodeling by hypoxia are strikingly different in arterial vs. venous endothelial cells. Our data have important implications for the interpretation of data obtained from endothelial cells of varying sources.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
No Reading authors. Back catalogue items
ID Code:30352
Uncontrolled Keywords:Ca2+; Hypoxia; Endothelium; Human tissue; Vein; Artery; Ca2+ influx; Ca2+ store
Publisher:Springer

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation