Angiotensin II interacts with prostaglandin F2α and endothelin-1 as a local luteolytic factor in the bovine corpus luteum in vitro
Angiotensin II interacts with prostaglandin F2α and endothelin-1 as a local luteolytic factor in the bovine corpus luteum in vitro
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DOI：
10.1095/biolreprod60.5.1104
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发表时间：
1999-05-01
影响因子：
3.6
通讯作者：
Miyamoto, A
中科院分区：
文献类型：
--
作者：
Hayashi, K;Miyamoto, A
最近的研究结果表明，卵巢肾素-血管紧张素系统可能通过血管紧张素 II (Ang II) 的旁分泌/自分泌作用来调节卵巢功能。在这项研究中，我们通过使用体外微透析系统（MDS），检查并表征了血管紧张素II作为黄体溶解因子的局部效应及其与黄体中期牛黄体（CL）中前列腺素F-2α（PGF（2α））和内皮素-1（ET-1）的相互作用。在MDS灌注液（4 pg/ml）中检测到Ang II，输注PGF（2α）（10（-6）M）2小时除了刺激ET-1释放外，在接下来的实验期间使Ang II释放增加50-100%。两次 2 小时输注 Ang II (10(-7)-10(-5) M)，间隔 2 小时，引起黄体酮 (P-4) 释放的剂量和时间依赖性减少 41-66%。当黄体外植体用PCF(10(-6)M)预灌注2小时时，以2小时间隔连续两次灌注Ang II(10(-6)M)迅速减少P-4释放(减少50%)。这种减少比单独输注 PGF(2α) 或 Ang II 早 6 小时。同时输注 1) Ang II (10(-6) M) 与 PGF(2 α) (10(-6) M)，2) ET-1 (10(-7) M) 与 PGF(2 α)，或 3) Ang II + ET-1 与 PGF(2 α) (10(-6) M) 2 小时也诱导 P-4 释放快速而显着 (60%) 减少。 Ang II 拮抗剂灌注可阻断单独 Ang II 或 PGF(2α) + Ang II 输注的 P-4 抑制活性。 Ang II 在输注过程中刺激 ET-1 和催产素的释放，但在输注后抑制它们。这些结果表明 Ang II 在体外牛周期中期 CL 中释放，并且该肽单独或与 PGF(2)α 一起可以抑制 P-4 的释放。由于PGF(2α)直接刺激Ang II释放，Ang II可能影响体内功能性黄体溶解级联启动的关键期，并可能导致以ET-1作为主要血管收缩剂的结构性黄体溶解。总体结果表明，Ang II 可能在牛 CL 的黄体溶解中发挥重要作用。
Recent findings suggest that the ovarian renin-angiotensin system may regulate ovarian function through the paracrine/autocrine actions of angiotensin II (Ang II). In this study, we have examined and characterized the local effects of Ang II as a luteolytic factor and its interaction with prostaglandin F-2 alpha (PGF(2 alpha)) and endothelin-1 (ET-1) in the bovine corpus luteum (CL) of the mid-luteal phase, by using an in vitro microdialysis system (MDS). Ang II was detected in the MDS perfusate (4 pg/ml), and infusion of PGF(2 alpha) (10(-6) M) for 2 h increased the Ang II release by 50-100% during the following experimental period, in addition to its stimulation of ET-1 release. Two 2-h infusions of Ang II (10(-7)-10(-5) M) separated by a 2-h interval induced a dose- and time-dependent decrease of progesterone (P-4) release by 41-66%. When the luteal explants were pre-perfused with PCF, (10(-6) M) for 2 h, two consecutive perfusions of Ang II (10(-6) M) at a 2-h interval rapidly reduced the P-4 release (by 50%). This reduction occurred 6 h earlier than those of infusions of PGF(2 alpha) or Ang II alone. The simultaneous infusion of either 1) Ang II (10(-6) M) with PGF(2 alpha) (10(-6) M), 2) ET-1 (10(-7) M) with PGF(2 alpha), or 3) Ang II + ET-1 with PGF(2 alpha) (10(-6) M) for 2 h also induced a rapid and pronounced (60%) decrease in P-4 release. Perfusion with the Ang II antagonist blocked the P-4-suppressing activity of Ang II alone or PGF(2 alpha) + Ang II infusion. Ang II stimulated the release of ET-1 and oxytocin during infusion but inhibited them after infusion.These results show that Ang II is released in the bovine midcycle CL in vitro, and this peptide, either alone or together with PGF(2)alpha, can suppress the release of P-4. As PGF(2 alpha) directly stimulated Ang II release, Ang II may influence the critical period for starting the cascade of functional luteolysis in vivo and might lead to structural luteolysis with ET-1 as a major vasoconstrictor. The overall results suggest that Ang II may have an important role at luteolysis in the bovine CL.