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

Isolated rabbit spinal resistance-sized arteries (approximately 100 microns in diameter and approximately 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 (delta P) ranging from 0 to 20 mmHg produced a flow-dependent vasodilation. Treatment with 50 microM aspirin or 10 microM indomethacin produced a significant reduction of the flow-dependent vasodilation only at delta P of 5 mmHg. In contrast, treatment with N omega-nitro-L-arginine methyl ester (L-NAME, 30 microM) produced no significant change. In the presence of 10 microM indomethacin, however, 30 microM L-NAME caused a marked decrease in the arterial diameter at delta 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 microM indomethacin or 50 microM aspirin and partially suppressed by 30 microM L-NAME. Pretreatment with both indomethacin and L-NAME completely reduced the ACh-induced vasodilation. In the presence of 10 microM 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.