Flow-mediated no release from endothelial cells is independent of
k+ channel activation or intracellular ca2+.
O'neill, W. Charles.
Renal Division, Department of Medicine, and Department of
Physiology, Emory University School of Medicine, Atlanta, GA
30322
APStracts 2:0173C, 1995.
The role of K+ channels and intracellular [Ca2+] in flow-induced 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 were grown
on collagen-coated microcarrier beads and perfused in a column. An 8
-fold increase in flow produced a rapid (within one minute),
sustained, and reversible 6-fold 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 later washout rather than to K+ channel activation since
an identical pattern was seen for release of [3H]ouabain. 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 is not dependent on
activation of K+ channels or changes in [Ca2+]i.
Received 26 January 1995; accepted in final form 11 April 1995.
APS Manuscript Number C51-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.