Chiba Y, Mikoda N, Kawasaki H, Ito K
Department of Veterinary Pharmacology, Faculty of Agriculture, Miyazaki University, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1990 Jan-Feb;341(1-2):68-73. doi: 10.1007/BF00195060.
Vasorelaxant action of platelet activating factor (PAF) was examined in perfused mesenteric vascular beds and mesenteric artery strips isolated from rats. PAF caused a dose-dependent vasodilation of norepinephrine-contracted mesenteric vascular bed, which was sensitive to CV-3988, a PAF antagonist, but insensitive to tetrodotoxin, atropine, propranolol and indomethacin. PAF also caused a relaxation of phenylephrine-contracted mesenteric artery strips at above 3 X 10(-12) M. Much higher concentrations of PAF were required to relax the aorta, carotid and pulmonary arteries. The PAF- and acetylcholine (ACh)-induced relaxations of mesenteric artery were dependent on the presence of endothelium and were inhibited by either hydroquinone and methylene blue, which inhibit the action of endothelium-derived relaxing factor (EDRF), or L-canavanine, which inhibits the formation of nitric oxide from L-arginine. Phospholipase A2 inhibitors such as quinacrine and ONO-RS-082 abolished the relaxation induced by ACh but did not affect that by PAF. Thus, PAF induces a vasorelaxation by releasing EDRF from endothelial cells as ACh does, although the pathway to produce the substances by PAF may be different from that by ACh.
在大鼠离体灌注肠系膜血管床和肠系膜动脉条上研究了血小板活化因子（PAF）的血管舒张作用。PAF可使去甲肾上腺素预收缩的肠系膜血管床产生剂量依赖性血管舒张，该作用对PAF拮抗剂CV-3988敏感，但对河豚毒素、阿托品、普萘洛尔和吲哚美辛不敏感。PAF在浓度高于3×10⁻¹² M时也可使苯肾上腺素预收缩的肠系膜动脉条舒张。使主动脉、颈动脉和肺动脉舒张则需要更高浓度的PAF。PAF和乙酰胆碱（ACh）诱导的肠系膜动脉舒张依赖于内皮细胞的存在，并且可被抑制内皮源性舒张因子（EDRF）作用的对苯二酚和亚甲蓝，或抑制L-精氨酸生成一氧化氮的L-刀豆氨酸所抑制。磷脂酶A2抑制剂如奎纳克林和ONO-RS-082可消除ACh诱导的舒张，但不影响PAF诱导的舒张。因此，PAF如同ACh一样，通过从内皮细胞释放EDRF诱导血管舒张，尽管PAF产生这些物质的途径可能与ACh不同。
