title: Flow- and agonist-mediated nitric oxide- and prostaglandin-dependent dilation in spinal arteries.
abstract: 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.
authors.affiliation: 1st Department of Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Yashiro
authors.forename: T
authors.initials: T
authors.lastname: Ohhashi
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D001241:Aspirin / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D011464:Epoprostenol / Q000031:analogs & derivatives / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D011312:Pressure; D011453:Prostaglandins / Q000502:physiology*; D011465:Prostaglandins, Synthetic / Q000494:pharmacology; D011817:Rabbits; D013131:Spine / Q000098:blood supply*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D011453:Prostaglandins; D011465:Prostaglandins, Synthetic; D016718:Arachidonic Acid; D009569:Nitric Oxide; C041946:9-O-methanoprostaglandin I; D011464:Epoprostenol; D015232:Dinoprostone; D000109:Acetylcholine; D001241:Aspirin; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin