Christian H C, Poyser N L
Department of Pharmacology, University of Edinburgh Medical School, UK.
Prostaglandins Leukot Essent Fatty Acids. 1994 Jul;51(1):57-62. doi: 10.1016/0952-3278(94)90179-1.
The initial, fast phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation (10 pulses) was dose-dependently and completely inhibited by prostaglandin (PG) E2, sulprostone and, at high concentrations, by cicaprost. Sulprostone was more potent than PGE2 indicating that the EP3 receptor was involved. Cicaprost (a PGI2 analogue) apparently had weak EP3 receptor against activity. At low concentrations, cicaprost potentiated the contractions of the vas deferens, presumably by acting on an IP receptor. Exogenous arachidonic acid also dose-dependently and completely inhibited contractions of the guinea-pig vas deferens. The action of arachidonic acid was delayed when compared to PGE2 and was inhibited by indomethacin, suggesting that the arachidonic acid was converted to PGE2 by the vas deferens. Indomethacin (1.4 to 6.0 microM) had no significant, potentiating effect on the contractions of the guinea-pig vas deferens which suggests that endogenous PGs do not normally inhibit this fast phase of contraction. In higher concentrations, the contractions were reduced by indomethacin. The fast phase of concentration of the guinea-pig vas deferens consisted of 3 components. PGE2, sulprostone and arachidonic acid inhibited all components. The order of inhibition of the components was component 2, then component 3, followed by component 1.
电场刺激（10个脉冲）引起的豚鼠输精管收缩的初始快速相，可被前列腺素（PG）E2、舒前列素以及高浓度时的西卡前列素剂量依赖性地完全抑制。舒前列素比PGE2更有效，表明涉及EP3受体。西卡前列素（一种前列环素类似物）显然对EP3受体的拮抗活性较弱。在低浓度时，西卡前列素可能通过作用于IP受体增强输精管的收缩。外源性花生四烯酸也剂量依赖性地完全抑制豚鼠输精管的收缩。与PGE2相比，花生四烯酸的作用延迟，且被吲哚美辛抑制，这表明花生四烯酸被输精管转化为PGE2。吲哚美辛（1.4至6.0微摩尔）对豚鼠输精管的收缩没有显著的增强作用，这表明内源性前列腺素通常不会抑制这种快速收缩相。在较高浓度时，吲哚美辛可使收缩减弱。豚鼠输精管收缩的快速相由3个成分组成。PGE2、舒前列素和花生四烯酸抑制所有成分。各成分的抑制顺序为成分2，然后是成分3，接着是成分1。
