Oxytocin and vasopressin constrict rat isolated uterine resistance arteries by activating vasopressin V1A receptors
Oxytocin and vasopressin constrict rat isolated uterine resistance arteries by activating vasopressin V1A receptors
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DOI：
10.1016/s0014-2999(99)00351-9
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发表时间：
1999-07-02
影响因子：
5
通讯作者：
Lai, FM
中科院分区：
文献类型：
--
作者：
Chen, YL;Shepherd, C;Lai, FM
催产素和加压素都能引起包括人类在内的被切断物种的子宫动脉强烈而持久的血管收缩，由此产生的组织缺血被认为参与了原发性痛经的发病机制。用选择性加压素V-1a受体拮抗剂SR-49059和催产素选择性拮抗剂阿托西班，研究了催产素和加压素对非妊娠大鼠子宫阻力动脉(直径90~120µm)的作用。将内皮完整的子宫动脉安装在微血管腔内，并将其加压至75 mm Hg以允许肌源性张力的形成。加压素和催产素均可引起浓度依赖的血管收缩，其最大效应相似(即完全阻断血管)。加压素和催产素的EC50分别为0.44+/-0.02和25+/-3.1 nM。因此，加压素的效力是催产素的57倍。SChild分析表明，SR 49059对加压素引起的收缩(pA(2)=8.96+/-0.60)和催产素引起的收缩(pA(2)=9.06+/-0.23)产生相似的pA(2)值，表明两种激动剂都激活了加压素V-1a受体。此外，大鼠催产素受体的选择性拮抗剂Atosiban(10(-7)M)不拮抗加压素和催产素的作用，表明催产素受体不参与这一反应。综上所述，这些结果提示，血管加压素和催产素对大鼠子宫小直径阻力动脉的收缩作用与刺激V-1a受体有关。(C)1999 Elsevier Science B.V.保留所有权利。
Both oxytocin and vasopressin cause potent and long-lasting vasoconstriction of uterine arteries from severed species, including humans, and the resulting tissue ischemia is thought to be involved in the pathogenesis of primary dysmenorrhea. We have studied the effects of oxytocin and vasopressin in isolated resistance arteries (diameter, 90-120 mu m) from non-pregnant rat uteri using two potent and selective receptor antagonists, SR 49059, a selective vasopressin V-1A antagonist, and atosiban, a selective oxytocin antagonist. Uterine arteries with intact endothelium were mounted in a microvessel chamber, and pressurized to 75 mm Hg to allow the development of myogenic tone. Both vasopressin and oxytocin elicited a concentration-dependent vasoconstriction with a similar maximum effect (i.e., total vessel occlusion). The EC50 was 0.44 +/- 0.02 and 25 +/- 3.1 nM for vasopressin and oxytocin, respectively. Thus, vasopressin was 57-fold more potent than oxytocin. Schild analysis indicated that SR 49059 yielded a similar pA(2) value against vasopressin-induced (pA(2) = 8.96 +/- 0.60) or oxytocin-induced (pA(2) = 9.06 +/- 0.23) contractions, suggesting that both agonists activated the vasopressin V-1A receptor. In addition, atosiban (10(-7) M), a selective antagonist of the oxytocin receptor in the rat, did not antagonize the effect of vasopressin and oxytocin, showing that the oxytocin receptor is not involved in the response. In conclusion, these results suggest that V-1A receptor stimulation is responsible for the vasoconstricting effects of both vasopressin and oxytocin in small diameter resistance arteries from the rat uterus. (C) 1999 Elsevier Science B.V. All rights reserved.