An eightfold increase in flow produced a rapid, sustained sixfold increase in NO release from endothelial cells that was independent of K+ channel activation or intracellular Ca2+.
Does flow-induced NO release depend on K+ channel activation or intracellular Ca2+ in bovine aortic endothelial cells?
Flow-mediated NO release from endothelial cells is independent of K+ channel activation or changes in intracellular Ca2+.
The role of K+ channels and intracellular Ca2+ in flow-induced nitric oxide (NO) production was investigated in bovine aortic endothelial cells in culture. NO release (measured as nitrite production) and K+ channel activity (measured as 86Rb+ efflux) were measured in cells grown on collagen-coated microcarrier beads and perfused in a column. An eightfold increase in flow produced a rapid (within 1 min), sustained, and reversible sixfold increase in NO release. Efflux of 86Rb+ also increased but rapidly returned to baseline and then transiently decreased when flow was decreased. This was probably due to boundary layer washout rather than to K+ channel activation, because an identical pattern was seen for release of 3Houabain. Neither tetraethylammonium nor increasing medium K+ to block K+ currents prevented flow-induced NO release. Removal of medium Ca2+ or chelation of intracellular Ca2+ also did not block flow-mediated NO release. The results demonstrate that flow rapidly increases NO release from endothelial cells but that this increase in NO release is not dependent on activation of K+ channels or changes in intracellular Ca2+.
W. Charles O’Neill (Sun,) conducted a other in Bovine aortic endothelial cells in culture. Increased flow vs. Baseline flow was evaluated on Nitric oxide (NO) release. An eightfold increase in flow produced a rapid, sustained sixfold increase in NO release from endothelial cells that was independent of K+ channel activation or intracellular Ca2+.