Arner M, Högestätt E D, Uski T K
Department of Hand Surgery, Malmö General Hospital, Sweden.
Acta Physiol Scand. 1991 Jan;141(1):79-86. doi: 10.1111/j.1748-1716.1991.tb09047.x.
The effects of prostaglandin F2 alpha, prostaglandin E1, prostaglandin E2 and the thromboxane A2 analogue U46619 were determined in ring segments of human hand veins. All prostanoids except prostaglandin E1 elicited contraction. The order of potency was U46619 greater than prostaglandin F2 alpha greater than prostaglandin E2. The thromboxane receptor antagonists BM13,505 and AH23848 both caused a parallel rightward displacement of the concentration-response curve for U46619 without depression of the maximum contraction, suggesting competitive antagonism. Schild plots for both antagonists yielded regression lines with slope indices not significantly different from unity. The pA2 values for BM13,505 and AH23848 were 7.9 and 8.4 respectively. Both antagonists also effectively inhibited prostaglandin F2 alpha-induced contractions. However, AH23848 significantly reduced the maximum response, and the results with BM13,505 gave no clear indication of the type of inhibition. In vein segments submaximally contracted by 5-hydroxytryptamine, prostaglandins E1 and E2 produced a biphasic response with a relaxation at low and a contraction at high concentrations. Prostaglandin F2 alpha and U46619 failed to elicit relaxation under these conditions. However, in the presence of either thromboxane receptor antagonist, prostaglandin F2 alpha but not U46619 produced a relaxation. The results are compatible with the presence of at least two prostanoid receptors in human hand veins, a contraction-mediating thromboxane receptor and an as yet unclassified receptor eliciting relaxation. U46619 was a potent agonist at the thromboxane receptor and prostaglandin E1 and E2 preferentially stimulated the relaxation-mediating receptor, whereas prostaglandin F2 alpha appeared to be active at both receptor sites.
在人手部静脉环段中测定了前列腺素F2α、前列腺素E1、前列腺素E2和血栓素A2类似物U46619的作用。除前列腺素E1外，所有前列腺素均引起收缩。效力顺序为U46619大于前列腺素F2α大于前列腺素E2。血栓素受体拮抗剂BM13505和AH23848均使U46619的浓度-反应曲线平行右移，而最大收缩未受抑制，提示为竞争性拮抗。两种拮抗剂的希尔德图产生的回归线斜率指数与1无显著差异。BM13505和AH23848的pA2值分别为7.9和8.4。两种拮抗剂也有效抑制前列腺素F2α诱导的收缩。然而，AH23848显著降低最大反应，而BM13505的结果未明确显示抑制类型。在由5-羟色胺引起次最大收缩的静脉段中，前列腺素E1和E2产生双相反应，低浓度时松弛，高浓度时收缩。在这些条件下，前列腺素F2α和U46619未能引起松弛。然而，在存在任何一种血栓素受体拮抗剂的情况下，前列腺素F2α而非U46619产生松弛。结果表明人手部静脉中至少存在两种前列腺素受体，一种介导收缩的血栓素受体和一种尚未分类的介导松弛的受体。U46619是血栓素受体的强效激动剂，前列腺素E1和E2优先刺激介导松弛的受体，而前列腺素F2α似乎在两个受体位点均有活性。
