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首页> 外文期刊>American Journal of Physiology >Localized accumulation of angiotensin II and production of angiotensin-(1-7) in rat luteal cells and effects on steroidogenesis.
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Localized accumulation of angiotensin II and production of angiotensin-(1-7) in rat luteal cells and effects on steroidogenesis.

机译：大鼠黄体细胞中血管紧张素II的局部积累和血管紧张素-（1-7）的产生及其对类固醇生成的影响。

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These studies aim to investigate subcellular distribution of angiotensin II (ANG II) in rat luteal cells, identify other bioactive angiotensin peptides, and investigate a role for angiotensin peptides in luteal steroidogenesis. Confocal microscopy showed ANG II distributed within the cytoplasm and nuclei of luteal cells. HPLC analysis showed peaks that eluted with the same retention times as ANG-(1-7), ANG II, and ANG III. Their relative concentrations were ANG II >or= ANG-(1-7) > ANG III, and accumulation was modulated by quinapril, an inhibitor of angiotensin-converting enzyme (ACE), Z-proprolinal (ZPP), an inhibitor of prolyl endopeptidase (PEP), and parachloromercurylsulfonic acid (PCMS), an inhibitor of sulfhydryl protease. Phenylmethylsulfonyl fluoride (PMSF), a serine protease inhibitor, did not affect peptide accumulation. Quinapril, ZPP, PCMS, and PMSF, as well as losartan and PD-123319, the angiotensin receptor type 1 (AT1) and type 2 (AT2) receptor antagonists, were used in progesterone production studies. ZPP significantly reduced luteinizing hormone (LH)-dependent progesterone production (P < 0.05). Quinapril plus ZPP had a greater inhibitory effect on LH-stimulated progesterone than either inhibitor alone, but this was not reversed by exogenous ANG II or ANG-(1-7). Both PCMS and PMSF acutely blocked LH-stimulated progesterone, and PCMS blocked LH-sensitive cAMP accumulation. Losartan inhibited progesterone production in permeabilized but not intact luteal cells and was reversed by ANG II. PD-123319 had no significant effect on luteal progesterone production in either intact or permeabilized cells. These data suggest that steroidogenesis may be modulated by angiotensin peptides that act in part through intracellular AT1 receptors.
机译：这些研究旨在调查血管紧张素II（ANG II）在大鼠黄体细胞中的亚细胞分布，鉴定其他具有生物活性的血管紧张素肽，并研究血管紧张素肽在黄体类固醇生成中的作用。共聚焦显微镜检查显示ANGII分布在黄体细胞的细胞质和细胞核内。 HPLC分析显示峰洗脱时间与ANG-（1-7），ANG II和ANG III相同。它们的相对浓度是ANG II>或= ANG-（1-7）> ANG III，并且积累是由奎那普利（血管紧张素转化酶（ACE）的抑制剂，Z-脯氨酸（ZPP），脯氨酰内肽酶的抑制剂）调节的（PEP）和对氯汞基磺酸（PCMS）（巯基蛋白酶的抑制剂）。苯甲基磺酰氟（PMSF），一种丝氨酸蛋白酶抑制剂，不影响肽的积累。奎纳普利，ZPP，PCMS和PMSF，以及氯沙坦和PD-123319、1型血管紧张素受体（AT1）和2型（AT2）受体拮抗剂被用于孕酮生产研究中。 ZPP显着降低了黄体生成激素（LH）依赖性孕激素的产生（P <0.05）。喹那普利加ZPP对LH刺激的孕激素的抑制作用要比单独使用任何一种抑制剂都要大，但是外源性ANG II或ANG-（1-7）并不能逆转这种抑制作用。 PCMS和PMSF均会急性阻断LH刺激的孕酮，而PCMS则会阻断LH敏感的cAMP积累。氯沙坦抑制透化的但不完整的黄体细胞中的孕激素产生，并被ANG II逆转。 PD-123319对完整或透化细胞中的黄体孕酮的产生没有明显影响。这些数据表明，类固醇生成可能受到血管紧张素肽的调节，该肽部分通过细胞内AT1受体起作用。

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