Flow- and agonist-mediated nitric oxide- and prostaglandin-dependent dilation in spinal arteries.

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 (ΔP) 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 ΔP of 5 mmHg. In contrast, treatment with N ω-nitro-l-arginine methyl ester (l-NAME, 30 μM) produced no significant change. In the presence of 10 μM indomethacin, however, 30 μMl-NAME caused a marked decrease in the arterial diameter at ΔP of 5 mmHg, which was completely reversed with additional administration of 1 mMl-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 μMl-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 mMl-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.