Hypoxia-induced increase in intracellular calcium concentration in endothelial cells: Role of the Na+-glucose cotransporter

2001 ◽  
Vol 84 (1) ◽  
pp. 115-131 ◽  
Author(s):  
Nancy Berna ◽  
Thierry Arnould ◽  
Jos� Remacle ◽  
Carine Michiels
1992 ◽  
Vol 152 (1) ◽  
pp. 215-221 ◽  
Author(s):  
Thierry Arnould ◽  
Carine Michiels ◽  
Isabelle Alexandre ◽  
Jos� Remacle

2006 ◽  
Vol 290 (6) ◽  
pp. H2498-H2508 ◽  
Author(s):  
D. Hong ◽  
D. Jaron ◽  
D. G. Buerk ◽  
K. A. Barbee

We investigated changes in calcium concentration in cultured bovine aortic endothelial cells (BAECs) and rat adrenomedulary endothelial cells (RAMECs, microvascular) in response to different levels of shear stress. In BAECs, the onset of shear stress elicited a transient increase in intracellular calcium concentration that was spatially uniform, synchronous, and dose dependent. In contrast, the response of RAMECs was heterogeneous in time and space. Shear stress induced calcium waves that originated from one or several cells and propagated to neighboring cells. The number and size of the responding groups of cells did not depend on the magnitude of shear stress or the magnitude of the calcium change in the responding cells. The initiation and the propagation of calcium waves in RAMECs were significantly suppressed under conditions in which either purinergic receptors were blocked by suramin or extracellular ATP was degraded by apyrase. Exogenously applied ATP produced similarly heterogeneous responses. The number of responding cells was dependent on ATP concentration, but the magnitude of the calcium change was not. Our data suggest that shear stress stimulates RAMECs to release ATP, causing the increase in intracellular calcium concentration via purinergic receptors in cells that are heterogeneously sensitive to ATP. The propagation of the calcium signal is also mediated by ATP, and the spatial pattern suggests a locally elevated ATP concentration in the vicinity of the initially responding cells.


1996 ◽  
Vol 118 (8) ◽  
pp. 1899-1904 ◽  
Author(s):  
Aida Salameh ◽  
Gunhild Schomecker ◽  
Katja Breitkopf ◽  
Stefan Dhein ◽  
Wolfgang Klaus

2010 ◽  
Vol 104 (3) ◽  
pp. 1216-1218 ◽  
Author(s):  
Ian Wenker

Recently, Henneberger and colleagues blocked hippocampal long-term synaptic potentiation (LTP) induction by “clamping” intracellular calcium concentration of individual CA1 astrocytes, suggesting calcium-dependent gliotransmitter release from astocytes plays a role in hippocampal LTP induction. However, using transgenic mice to manipulate astrocytic calcium, Agulhon and colleagues demonstrated no effect on LTP induction. Until the question of how intracellular calcium causes gliotransmitter release is answered, the role of astrocytes in synaptic plasticity will be incompletely understood.


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