Fahey J V, Newcombe D S
Inflammation. 1979 Jul;3(3):235-42. doi: 10.1007/BF00914180.
Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids. Both these bradykinin-induced reactions are inhibited by quinacrine, an inhibitor of phospholipase A activity. The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha. These data emphasize the critical role of the prostaglandin system in reactions induced by bradykinin and suggest mechansims by which inflammatory reactions due to bradykinin may be modulated.
缓激肽可使人类滑膜成纤维细胞内的环磷酸腺苷（cAMP）浓度升高，并促使预先用磷脂标记的人类滑膜成纤维细胞释放[3H]花生四烯酸和[3H]-E前列腺素。缓激肽诱导的这两种反应均被磷脂酶A活性抑制剂奎纳克林所抑制。前列腺素E2可增强人类滑膜成纤维细胞对缓激肽的环磷酸腺苷反应，而前列腺素F2α则可抑制该反应。这些数据强调了前列腺素系统在缓激肽诱导的反应中的关键作用，并提示了缓激肽引起的炎症反应可能的调节机制。
