Cyclic nucleotides and Ca2+ influx pathways in vascular endothelial cells.
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.
Kwan
H Y
HY
Department of Physiology, The Chinese University of Hong Kong, Hong Kong, China.
Huang
Y
Y
Yao
X
X
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology; D017869:Cyclic GMP-Dependent Protein Kinases / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D009712:Nucleotides, Cyclic / Q000378:metabolism*; D014664:Vasodilation
D009712:Nucleotides, Cyclic; D017869:Cyclic GMP-Dependent Protein Kinases; D002118:Calcium