Cyclic nucleotides and Ca 2+ influx pathways in vascular endothelial cells

Abstract

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.