Affiliations: Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong | Department of Pharmacology and Pharmacy, University of Bath, Bath BA2 7AY, UK
Note: [] Address for correspondence: Xiaoqiang Yao, Ph.D., Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, Hong Kong. Tel.: 852 26096877; Fax: 852 26035022; E‐mail: [email protected].
Abstract: Ca2+ is an important intracellular second messenger in signal transduction of endothelial cells. It has long been recognized that a mechanosensitive Ca2+‐permeable channel is present in vascular endothelial cells. The activity of this channel may increase intracellular Ca2+ level in endothelial cells. A recent finding is that the activity of this channel may be regulated by cGMP through a protein kinase G‐dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+, Ni2+, and SK&F‐96365 also inhibit the Ca2+ influx due to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow‐induced Ca2+ entry in vascular endothelial cells. Another important finding is that the opening of this mechanosensitive channel by KT5823 leads to endothelium‐dependent vascular dilation. Therefore, it appears that this channel may play a crucial role in the regulation of vascular tone.
Journal: Biorheology, vol. 40, no. 1-3, pp. 23-30, 2003
