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The 1st Department of Physiology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390, Japan
Isolated rabbit spinal resistance-sized
arteries (~100 µm in diameter and ~3 mm long) were cannulated at
both ends with glass micropipettes and perfused at constant pressure
(60 mmHg). An increase of flow rate corresponding to a
change of pressure gradient (
P) ranging from 0 to 20 mmHg produced a
flow-dependent vasodilation. Treatment with 50 µM aspirin or 10 µM
indomethacin produced a significant reduction of the flow-dependent
vasodilation only at
P of 5 mmHg. In contrast, treatment with
N
-nitro-L-arginine
methyl ester (L-NAME, 30 µM)
produced no significant change. In the presence of 10 µM
indomethacin, however, 30 µM L-NAME caused a marked decrease
in the arterial diameter at
P of 5 mmHg, which was completely
reversed with additional administration of 1 mM
L-arginine. Acetylcholine (ACh)
produced a dose-dependent increase in the arterial diameter. The
ACh-induced vasodilation was significantly reduced by 10 µM
indomethacin or 50 µM aspirin and partially suppressed by 30 µM
L-NAME. Pretreatment with both indomethacin and L-NAME
completely reduced the ACh-induced vasodilation. In the presence of 10 µM indomethacin, additional treatment with 1 mM
L-arginine significantly
reversed the L-NAME-induced
inhibition of the ACh-mediated vasodilation. Endothelial removal with
Triton X-100 significantly reduced the ACh-induced vasodilation.
Isocarbacyclin (a stable prostaglandin
I2 analogue), prostaglandin
E2, and arachidonic acid caused a
dose-dependent dilation in the small arteries. These findings suggest
that prostanoids play a major role in the flow- or ACh-induced
vasodilation in the rabbit spinal resistance-sized small arteries.
spine; resistance-sized small artery; shear stress; acetylcholine; endothelium-derived relaxing factors
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