Cyclic nucleotides and Ca2+ influx pathways in vascular endothelial cells
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Updated: Jul 13, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
Published on: July 16, 2013
1Department of Physiology, The Chinese University of Hong Kong, Hong Kong, China.
Abstract:
Ca(2+) mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca(2+) [Ca(2+)](i), which then acts to stimulate nitric oxide synthase and phospholipase A(2), leading to the production and release of nitric oxide (NO) and other vascular substances such as prostacyclin and endothelium-derived hyperpolarizing factors (EDHF). In this article, regulatory mechanisms of agonist-induced and mechanosensitive Ca(2+) influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca(2+) influx by protein kinase G (PKG). Flow-induced Ca(2+) influx in relation to vascular dilation and the vasodilator produced will also be discussed.
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