首页> 外文期刊>Reproduction, fertility, and development >Angiotensin II increases intracellular calcium concentration in pig endometrial stromal cells through type 1 angiotensin receptors, but does not stimulate phospholipase C activity or prostaglandin F2alpha secretion.
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Angiotensin II increases intracellular calcium concentration in pig endometrial stromal cells through type 1 angiotensin receptors, but does not stimulate phospholipase C activity or prostaglandin F2alpha secretion.

机译:血管紧张素II通过1型血管紧张素受体增加猪子宫内膜基质细胞的细胞内钙浓度,但不刺激磷脂酶C活性或前列腺素F2alpha分泌。

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Although the presence of endometrial receptors for angiotensin (Ang) II has been demonstrated, a specific function for AngII in the uterus has not been identified. Cytosolic free Ca2+ concentration [Ca2+]i, phospholipase C (PLC) activity and prostaglandin (PG) F2alpha secretion in response to AngII and oxytocin (OT) were measured in pig endometrial stromal cells collected 16 days after oestrus. Treatment with 100 nM OT or AngII increased (P<0.001) [Ca2+]i in stromal cells similarly (720 +/- 34 v. 690 +/- 33 pM, respectively). Subsequent administration of OT or AngII to the same cells induced smaller [Ca2+]i increases (25% or 35% of the initial responses, respectively) that occurred only if the second exposure to the same agent took place at least 5 min after the first. When administered sequentially, OT and AngII each induced a full response within 1 min of the previous treatment, regardless of which peptide was applied first. Whereas OT increased PLC activity and PGF2alpha secretion in stromal cells (P<0.01), AngII did not increase either PLC activity or PGF2alpha secretion. Type I AngII (AT1) receptors were present on stromal cells, whereas AT2 receptors were absent. Therefore, the effect of AngII in stromal cells was mediated via AT1 receptors. That AngII increased [Ca2+]i in stromal cells, but did not increase PLC or PGF2alpha secretion, indicates that either AngII releases a pool of Ca2+ through a mechanism that is not mediated by PLC and is not involved in PGF2alpha secretion or that a mechanism for PGF2alpha production other than one involving Ca2+ may exist.
机译:尽管已证实血管紧张素(Ang)II的子宫内膜受体的存在,但尚未确定AngII在子宫中的特定功能。在发情16天后收集的猪子宫内膜基质细胞中,测量了对AngII和催产素(OT)的响应,细胞内游离Ca2 +浓度[Ca2 +] i,磷脂酶C(PLC)活性和前列腺素(PG)F2α分泌。用100 nM OT或AngII进行治疗,基质细胞中[Ca2 +] i的升高幅度相似(分别为720 +/- 34 v。690 +/- 33 pM)。随后对相同细胞施用OT或AngII会引起较小的[Ca2 +] i升高(分别是初始反应的25%或35%),只有在第一次暴露于同一药物后至少5分钟进行第二次暴露时才会发生。当顺序给药时,OT和AngII均在上次治疗后1分钟内诱导完全应答,无论首先使用哪种肽。 OT增加基质细胞中PLC活性和PGF2α分泌(P <0.01),而AngII既不增加PLC活性也不增加PGF2α分泌。 I型AngII(AT1)受体存在于基质细胞上,而AT2受体不存在。因此,AngII在基质细胞中的作用是通过AT1受体介导的。 AngII增加基质细胞中[Ca2 +] i,但不增加PLC或PGF2alpha分泌,这表明AngII通过非PLC介导且不参与PGF2alpha分泌的机制释放Ca2 +池,或可能存在除涉及Ca2 +的一种以外的PGF2alpha产生。

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