Blood flow: A key regulatory component of corpus luteum function in the cow
Blood flow: A key regulatory component of corpus luteum function in the cow
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DOI：
10.1016/j.domaniend.2005.03.011
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发表时间：
2005-08-01
影响因子：
2.1
通讯作者：
Acosta, TJ
中科院分区：
文献类型：
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作者：
Miyamoto, A;Shirasuna, K;Acosta, TJ
前列腺素 F2 α (PGF(2a)) 是牛体内的主要木黄素溶血素。在黄体早期，黄体 (CL) 对 PGF(2a) 的黄体分解作用具有抵抗力。一旦成熟，CL 就会对 PGF(2α) 产生反应。并经历黄体退化。 PGF(2α) 的这些作用与黄体血流量 (BF) 的变化相一致：PGF(2α) 对早期 CL 中的 BF 没有影响，但在注射 PGF(2α) 后 30 分钟内，成熟 CL 的外周血管系统中的 BF 急剧增加。在自发性黄体溶解期间，黄体 BF 在动情周期第 17-18 天增加，然后血浆孕酮 (P) 减少。黄体 BF 的增加与血浆 PGFM 水平的增加同步，表明子宫脉冲式释放 PGF(2α) 刺激黄体 BE 的增加。这些 CL 的连续活检显示，当黄体 BF 增加时，内皮一氧化氮合酶 (eNOS) 以及内皮素-1 (ET-1) 和血管紧张素转换酶 (ACE) 的 mRNA 表达在第 17-18 天增加。是升高的。第19天，血浆P水平首先下降，eNOS mRNA恢复至基础水平，而ET-1和ACE mRNA仍然升高。第 19 天，环氧合酶-2 (COX-2) mRNA 表达增加。为了支持这些数据，体内微透析研究表明，黄体 ET-1 和血管紧张素 II (Ang II) 分泌增加，且先于 PGF2。自发性黄体溶解过程中的分泌。总之，我们首次表明，在牛黄体溶解的早期阶段，成熟 CL 的外周脉管系统中 BF 急剧增加，同时 CL 中 eNOS 表达以及 ET-1 和 Ang II 分泌增加。我们认为黄体BF的增加可能是由CL周围大动脉的NO诱导的，同时子宫或外源性PGF(2a)直接增加CL内微毛细血管内皮细胞的ET-1和Ang II分泌，从而抑制黄体细胞的P分泌。总而言之，我们的结果表明，黄体 BF 急剧增加是响应 PGF(2 α) 黄体溶解的第一步。因此，局部 BF 在奶牛黄体退化的启动中起着关键作用。 (c) 2005 Elsevier Inc. 保留所有权利。
Prostaglandin F2 alpha (PGF(2a)) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF(2a), Once mature, the CL becomes responsive to PGF(2 alpha). and undergoes luteal regression. These actions of PGF(2 alpha) coincide with changes in luteal blood flow (BF): PGF(2 alpha) has no effect on BF in the early CL, but acutely increases BF in the peripheral vasculature of the mature CL within 30 min of PGF(2 alpha) injection. During spontaneous luteolysis, luteal BF increases on Days 17-18 of the estrous cycle, prior to any decrease in plasma progesterone (P). The increase in luteal BF is synchronous with an increase in plasma PGFM levels, suggesting that pulsatile release of PGF(2 alpha) from uterus stimulates the increase in luteal BE Serial biopsies of these CL showed that mRNA expression for endothelial nitric oxide synthase (eNOS) together with endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) increases on Days 17-18 when the luteal BF is elevated. On Day 19 when plasma P level firstly decreases, eNOS mRNA returns to the basal level whereas ET-1 and ACE mRNA remains elevated. Cyclooxygenase-2 (COX-2) mRNA expression increases on Day 19. In support of these data, an in vivo microdialysis study revealed that luteal ET-1 and angiotensin II (Ang II) secretion increases and precedes PGF2. secretion during spontaneous luteolysis. In conclusion, we show for the first time that an acute increase of BF occurs in the peripheral vasculature of the mature CL together with increases in eNOS expression and ET-1 and Ang II secretion in the CL during the early stages of luteolysis in the cow. We propose that the increase in luteal BF may be induced by NO from large arterioles surrounding the CL, and simultaneously uterine or exogenous PGF(2a) directly increases ET-1 and Ang II secretion from endothelial cells of microcapillary vessels within the CL, thereby suppressing P secretion by luteal cells. Taken together, our results indicate that an acute increase in luteal BF occurs as a first step of luteolysis in response to PGF(2 alpha). Therefore, local BF plays a key role to initiate luteal regression in the cow. (c) 2005 Elsevier Inc. All rights reserved.