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Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki 036-8562, Japan
We tested the
hypothesis that vessel homeostasis is maintained through the cross talk
of shear-induced production of prostacyclin and nitric oxide (NO).
Confluent human umbilical vein endothelial cells (HUVEC) were exposed
to fluid shear stress at 15 dyn/cm2 using a cone-plate
device, and the concentrations of 6-keto-PGF1
and NO
metabolites (nitrate and nitrite) in the medium were measured with
radioimmunoassay and the Greiss method, respectively. Compared with
static control, shear stress increased cumulative prostacyclin production by twofold after 90 min of exposure. Inhibition of NO
synthase enhanced flow-induced prostacyclin production by twofold without affecting the baseline production. Guanylyl cyclase inhibitor enhanced flow-induced prostacyclin production to the same degree. In
contrast, a stable agonist of cGMP attenuated the rapid early phase of
flow-dependent prostacyclin production. Shear-induced NO metabolite
production was unaffected even after indomethacin inhibited
prostacyclin production. We conclude that NO shows an inhibitory effect
on prostacyclin production under shear stress and that vessel
homeostasis may be maintained through an increase in prostacyclin
production when NO synthesis is impaired in endothelial cells.
shear stress; guanosine 5'-triphosphate-binding protein; guanosine 3',5'-cyclic monophosphate
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