Location
Philadelphia Campus
Start Date
2-5-2012 2:00 PM
End Date
2-5-2012 4:00 PM
Description
Background: Leukocyte-endothelial interactions associated with vascular injury are attenuated by endothelial-derived nitric oxide (NO). Endothelial NO synthase (eNOS) in the presence of tetrahydrobiopterin (BH4) produces NO from L-arginine and is termed eNOS coupling. However, when the ratio of dihydrobiopterin (BH2) to BH4 is increased, eNOS becomes uncoupled and produces superoxide instead of NO. Protein kinase C epsilon (PKC ε) positively regulates eNOS activity. This study examined modulating eNOS activity and coupling by superfusing BH2 (100 μM) by itself, combined with PKC ε activator (10μM) or PKC ε inhibitor, or combined with BH4 (100μM) and PKC ε activator in rat mesenteric venules.
The Effects of Modulating eNOS Activity and Coupling on Leukocyte-endothelial Interactions in Rat Mesenteric Postcapillary Venules
Philadelphia Campus
Background: Leukocyte-endothelial interactions associated with vascular injury are attenuated by endothelial-derived nitric oxide (NO). Endothelial NO synthase (eNOS) in the presence of tetrahydrobiopterin (BH4) produces NO from L-arginine and is termed eNOS coupling. However, when the ratio of dihydrobiopterin (BH2) to BH4 is increased, eNOS becomes uncoupled and produces superoxide instead of NO. Protein kinase C epsilon (PKC ε) positively regulates eNOS activity. This study examined modulating eNOS activity and coupling by superfusing BH2 (100 μM) by itself, combined with PKC ε activator (10μM) or PKC ε inhibitor, or combined with BH4 (100μM) and PKC ε activator in rat mesenteric venules.