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Focal agonist stimulation results in spatially restricted Ca²⁺ release and capacitative Ca²⁺ entry in bovine vascular endothelial cells

Jörg Hüser, Jaclyn R. Holda, Jens Kockskämper and Lothar A. Blatter

Intracellular Ca²⁺ ([Ca²⁺]_i) signals were studied with spatial resolution in bovine vascular endothelial cells using the fluorescent Ca²⁺ indicator fluo-3 and confocal laser scanning microscopy. Single cells were stimulated with the purinergic receptor agonist ATP resulting in an increase of [Ca²⁺]_i due to intracellular Ca²⁺ release from inositol 1,4,5-trisphosphate (IP₃)-sensitive stores. ATP-induced Ca²⁺ release was quantal, i.e. submaximal concentrations mobilized only a fraction of the intracellularly stored Ca²⁺.

Focal receptor stimulation in Ca²⁺-free solution by pressure application of agonist-containing solution through a fine glass micropipette resulted in a spatially restricted increase in [Ca²⁺]_i. Ca²⁺ release was initiated at the site of stimulation and frequently propagated some tens of micrometres into non-stimulated regions.

Local Ca²⁺ release caused activation of capacitative Ca²⁺ entry (CCE). CCE was initially colocalized with Ca²⁺ release. Following repetitive focal stimulation, however, CCE became detectable at remote sites where no Ca²⁺ release had been observed. In addition, the rate of Ca²⁺ store depletion with repetitive local activation of release in Ca²⁺-free solution was markedly slower than that elicited by ATP stimulation of the entire cell.

From these experiments it is concluded that both intracellular IP₃-dependent Ca²⁺ release and activation of CCE are controlled locally at the subcellular level. Moreover, redistribution of intracellular Ca²⁺ stored within the endoplasmic reticulum efficiently counteracts local store depletion and accounts for the spatial spread of CCE activation.

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