Ca2+ mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca2+ [Ca2+] i, which then acts to stimulate nitric oxide synthase and phospholipase A2, 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 Ca2+ influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca2+ influx by protein kinase G (PKG). Flow-induced Ca2+ influx in relation to vascular dilation and the vasodilator produced will also be discussed.
|Number of pages||8|
|Journal||Clinical Hemorheology and Microcirculation|
|Publication status||Published - Jan 2007|
Scopus Subject Areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)