Circulation, Vol 85, 2284-2290, Copyright © 1992 by American Heart Association
JC de Graaf, JD Banga, S Moncada, RM Palmer, PG de Groot and JJ Sixma
BACKGROUND. Nitric oxide (NO) has been identified as endothelium- derived
relaxing factor (EDRF), which, in addition to its relaxant effects on
vascular smooth muscle cells, is also a potent inhibitor of platelet
aggregation. An inhibitory role on platelet adhesion has been suggested
from experiments with washed platelets under static conditions. We have
determined whether endothelium-derived and exogenous NO also regulates
platelet adhesion in whole blood under flow conditions. METHODS AND
RESULTS. The effect of endothelium-derived NO was studied by the addition
of specific inhibitors of NO production, L- N-monomethyl arginine (L-NMMA)
and N-iminoethyl-L-ornithine (L-NIO), to a perfusion system in which both
endothelial cells and their matrices were present. A
concentration-dependent increase in platelet adhesion to the matrix was
found with a maximum inhibition at a concentration of 2 mM L-NMMA and 0.1
mM L-NIO. The effect was dependent on the presence of endothelial cells,
because no increase in platelet adhesion was observed in their absence. The
effect of exogenous NO was tested in a specially devised perfusion system
in which the NO was introduced at the site of adhesion by means of a porous
membrane on which an extracellular matrix of endothelial cells was present.
Inhibition of platelet adhesion by NO was found at all shear rates tested
and after all perfusion periods. CONCLUSIONS. These results demonstrate
that NO is a potent inhibitor of platelet adhesion under flow conditions
and thereby contributes to the regulatory role of vascular endothelial
cells on platelet-vessel wall interaction.
ARTICLES
Nitric oxide functions as an inhibitor of platelet adhesion under flow conditions
Department of Hematology, University Hospital Utrecht, The Netherlands.
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