Related Experiment Videos
Endothelial cell thromboxane production and its inhibition by a calcium-channel blocker
F M Ramadan1, G R Upchurch, B A Keagy
1Department of Surgery, University of North Carolina, Chapel Hill, NC 27599-7210.
Vascular endothelium has been established as a major source of prostacyclin production. Whether endothelial cells are also capable of synthesizing thromboxane A2 remains controversial. Suppression of such endothelial thromboxane synthesis would be beneficial for short-term patency of vascular grafts. This study examined the production of thromboxane A2 by endothelial cells and its modulation by the calcium-channel blocker nifedipine in vitro. The results indicate that (1) endothelial cells spontaneously secrete thromboxane A2, (2) this production can be enhanced severalfold in the presence of arachidonic acid, and (3) the calcium-channel blocker nifedipine significantly inhibits thromboxane production without demonstrable toxicity to the endothelial cells.
Vascular endothelium has been established as a major source of prostacyclin production. Whether endothelial cells are also capable of synthesizing thromboxane A2 remains controversial. Suppression of such endothelial thromboxane synthesis would be beneficial for short-term patency of vascular grafts. This study examined the production of thromboxane A2 by endothelial cells and its modulation by the calcium-channel blocker nifedipine in vitro. The results indicate that (1) endothelial cells spontaneously secrete thromboxane A2, (2) this production can be enhanced severalfold in the presence of arachidonic acid, and (3) the calcium-channel blocker nifedipine significantly inhibits thromboxane production without demonstrable toxicity to the endothelial cells.