2 POOLS OF PITUITARY GONADOTROPIN - REGULATION DURING MENSTRUAL-CYCLE
2 POOLS OF PITUITARY GONADOTROPIN - REGULATION DURING MENSTRUAL-CYCLE
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DOI：
10.1210/jcem-44-2-302
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发表时间：
1977-01-01
影响因子：
5.8
通讯作者：
YEN, SSC
中科院分区：
文献类型：
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作者：
HOFF, JD;LASLEY, BL;YEN, SSC
通过4小时LRF [促黄体生成激素释放激素]输注（0.2 μ g/min × 100 μ g/min）获得关于在正常月经周期期间垂体LH [促黄体生成激素]的急性释放（第一）和储备（第二）库之间的相对活性和功能关系的信息。4 h）。随后立即进行3次LRF脉冲（10 μ g，间隔2小时），以进一步评估通过输注激活储备库后急性可释放库的大小。两个功能池的LH显然是存在于月经周期的各个阶段，比较池的大小或活动可能是深刻的影响卵巢类固醇反馈和下丘脑LRF的输入模式。从早期到晚期卵泡期，与E2 [雌二醇]水平的上升同步，第二池的大小优先增加。第一池活性的小幅增加不明显，直到卵泡晚期，此时第二池的大小也增加了5倍。在黄体中期，与相对较高的孕酮（P）和E2相关，大的第二池保持在卵泡晚期，但第一池明显较小。与未输注对照相比，通过LRF输注（预充）激活第2个LH池可增加周期所有3个阶段中的急性释放LH（第1个池），如输注结束时对第1个但非后续LRF脉冲的反应增强所证明。这种启动效应可能反映了LH从较大的第二池到较小的第一池的激活或转移。与其他周期阶段相比，这种促发作用在黄体中期最大。在周期中期LH激增期间，观察到2个池的相对活性的急剧逆转，表现为第1个池相对于第2个池的活性的巨大增加。与其他周期阶段相反，第二池的LH释放不持续。尽管持续输注LRF，但LH释放的过早下降似乎是由于垂体LH耗竭，如输注后立即对LRF脉冲的垂体反应失败所证明。LRF可能不仅诱导LH的合成-储存（第二池）和释放（第一池），而且激活第二池，使其LH更容易释放。这些积极的影响所施加的LRF可能被放大的E2的存在，这似乎提供了一个许可的行动LRF，除了E2也起到阻碍LRF介导的LH释放。黄体中期的P水平可能不会抑制E2引起的第二池的增加，但可能会放大LRF诱导的第二池的激活，同时扩大较小的第一池。在周期中期，假定增加内源性LRF释放和雌激素依赖性LRF自吸效应的发展可能会导致LH从第二池急剧转移到第一池，并通过克服E2的阻碍作用加速LH释放。
Information on the relative activity and on functional relationships between the acutely releasable (1st) and reserve (2nd) pools of pituitary LH [luteinizing hormone] during the normal menstrual cycle was obtained via a 4 h LRF [luteinizing hormone-releasing hormone] infusion (0.2 .mu.g/min .times. 4 h). This was immediately followed by 3 pulses of LRF (10 .mu.g at 2 h intervals) to assess further the size of the acutely releasable pool after activation of the reserve pool by the infusion. Two functional pools of LH are apparently present in all phases of the menstrual cycle, and comparative pool size or activity is probably influenced profoundly by ovarian steroid feedback and by the pattern of input of hypothalamic LRF. From the early to the late follicular phase, in synchrony with the rising levels of E2 [estradiol], the size of the 2nd pool is preferentially augmented. A small increase in the 1st pool activity is not apparent until the late follicular phase when a 5-fold increase in the size of the 2nd pool is also attained. During the mid-luteal phase and in association with relatively high progesterone (P) and E2, the large 2nd pool is maintained as in the late follicular phase, but the 1st pool is strikingly smaller. Activation of the 2nd pool of LH by LRF infusion (priming) increases the acutely releasable LH (1st pool) in all 3 phases of the cycle, as evidenced by an enhanced response to the 1st but not subsequent pulses of LRF at the end of the infusion, as compared with non-infused controls. This priming effect probably reflects activation or shifting of LH from the larger 2nd pool to the smaller 1st pool. This priming effect is greatest during the mid-luteal phase as compared to other cycle phases. During the mid-cycle LH surge, a dramatic reversal of the relative activity of the 2 pools is observed, manifested by an enormous increase in the activity of the 1st relative to the 2nd pool. In contrast to other cycle phases, LH release from the 2nd pool is not sustained. This premature decline in LH release despite continuous LRF infusion appears to be due to pituitary depletion of LH, as evidenced by the failure of the pituitary response to pulses of LRF immediately following the infusion. LRF probably not only induces synthesis-storage (2nd pool) and release (1st pool) of LH, but also activates the 2nd pool and renders its LH more readily releasable. These positive influences exerted by LRF are probably amplified by the presence of E2 which appears to provide a permissive action of LRF, except E2 also functions to impede the LRF mediated LH-release. Mid-luteal levels of P probably do not inhibit the augmented 2nd pool due to E2 but may amplify the LRF induced activation of the 2nd pool with enlargement of the smaller 1st pool. At mid-cycle, the assumed increased endogenous LRF release and the development of estrogen dependent self-priming effect of LRF probably induces a dramatic shifting of LH from the 2nd to the 1st pool with accelerated LH release by overcoming the impeding action of E2.