Cyclic nucleotides and Ca²⁺ influx pathways in vascular endothelial cells

Issue title: Selected Papers from 1st Meeting on “Cardiovascular Biology: Endothelial Cell in Health and Hypertension”, 30 June–1 July 2006, Prague, Czech Republic

Article type: Research Article

Authors: Kwan, H.Y. | Huang, Y. | Yao, X.

Affiliations: Department of Physiology, The Chinese University of Hong Kong, Hong Kong, China

Note: [] Corresponding author: X. Yao, Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China. E-mail: [email protected].

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.

Journal: Clinical Hemorheology and Microcirculation, vol. 37, no. 1-2, pp. 63-70, 2007