Stewart A G, Dubbin P N, Harris T, Dusting G J
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
Br J Pharmacol. 1989 Mar;96(3):503-5. doi: 10.1111/j.1476-5381.1989.tb11845.x.
Bovine culture endothelial cells (BAECs) generate platelet-activating factor (Paf) following activation by bradykinin (Bk 0.1 nM), the ionophore, A23187 (3 microM), and ATP (10 microM), but Paf is not released from the cells. These stimuli also elicit generation of prostacyclin (PGI2). The specific and competitive Paf receptor antagonists, WEB 2086 (0.1-1.0 microM) and CV 6209 (0.01-0.1 microM), inhibited Bk-, A23187- and, to a lesser extent, ATP-induced PGI2 generation but had no effect on basal PGI2 generation. These data suggest a role for intracellular Paf in signal transduction.
牛主动脉内皮细胞(BAECs)在被缓激肽(Bk 0.1 nM)、离子载体A23187(3 microM)和ATP(10 microM)激活后会产生血小板活化因子(Paf),但Paf不会从细胞中释放出来。这些刺激也会引发前列环素(PGI2)的生成。特异性和竞争性的Paf受体拮抗剂WEB 2086(0.1 - 1.0 microM)和CV 6209(0.01 - 0.1 microM)可抑制Bk、A23187以及在较小程度上抑制ATP诱导的PGI2生成,但对基础PGI2生成没有影响。这些数据表明细胞内Paf在信号转导中发挥作用。