Response of the magnocellular system in rats to hypovolemia and cholecystokinin during pregnancy and lactation.
Response of the magnocellular system in rats to hypovolemia and cholecystokinin during pregnancy and lactation.
复制标题
妊娠和哺乳期间大鼠大细胞系统对低血容量和胆囊收缩素的反应。
DOI：
10.1152/ajpregu.1994.266.4.r1327
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Summy-Long,JY
中科院分区：
文献类型：
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作者：
Koehler,EM;McLemore,GL;Martel,JK;Summy-Long,JY
为了明确哺乳期和妊娠期大细胞神经内分泌系统的变化，我们比较了聚乙二醇(PEG)诱导的低血容量和胆囊素(CCK)刺激后血浆催产素(OT)和加压素(VP)的水平。清醒的处女、妊娠(第20天)和哺乳期(第6天)的SD大鼠分别注射聚乙二醇(70-600 mg/ml；35或70ml/kg sc)、CCK(100微克/ml；4ml/kg ip)或赋形剂，4h或5min后断头处死。使用迭代的非线性阈值回归模型确定OT和VP系统的激素释放阈值和反应性(与血容量耗竭或血浆渗透压有关的斜率)。在聚乙二醇组，血浆渗透压升高与血容量减少一致，这两种刺激均导致血浆VP和OT升高。与未孕大鼠相比，联合刺激不改变VP系统的阈值和反应性，而孕鼠的催产素能系统对渗透压成分的反应更强。然而，哺乳期大鼠的VP释放阈值较高，OT阈值明显升高，超过25%的容量耗竭。无论生殖状态如何，VP释放的阈值始终低于OT。尽管在哺乳期动物的反应减弱，但在每种生殖状态下，腹膜内CCK使血浆[OT]升高。在处女鼠和哺乳期大鼠，血浆VP水平也略有升高，但对CCK的反应显著。在妊娠期间，当心血管容量扩大时，VP和OT神经内分泌系统都被重置，使这两种激素能够分泌，以应对高张低血症。在哺乳期间，两个神经内分泌系统都被重置，因此需要更大的体液平衡变化来刺激激素释放。无论生殖状态如何，VP释放的阈值总是低于OT，这表明VP优先释放，血容量损失小于5%(处女、怀孕)或20%(哺乳期)。
To define changes in the magnocellular neuroendocrine system during lactation and pregnancy, we compared plasma levels of oxytocin (OT) and vasopressin (VP) after polyethylene glycol (PEG)-induced hypovolemia and cholecystokinin (CCK) stimulation. Conscious virgin, pregnant (day 20), and lactating (day 6) Sprague-Dawley rats were injected with either PEG (70-600 mg/ml; 35 or 70 ml/kg sc), CCK (100 micrograms/ml; 4 ml/kg ip), or vehicle and decapitated 4 h (PEG) or 5 min (CCK) later. Changes in thresholds for release of hormone and the responsiveness (slopes relating [hormone] to blood volume depletion or to plasma osmolality) of the OT and VP systems were determined using an iterative nonlinear threshold regression model. After PEG, plasma osmolality increased coincident with a decrease in blood volume, with both stimuli contributing to the rise in plasma VP and OT. Compared with virgin rats, neither the threshold nor the responsiveness of the VP system was altered by the combined stimulus, whereas the oxytocinergic system of pregnant rats was more responsive to osmotic component. Lactating rats, however, had a higher threshold for VP release and an apparent elevation of the OT threshold beyond 25% volume depletion. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT. Intraperitoneal CCK elevated plasma [OT] in each reproductive state, although the response in lactating animals was attenuated. In virgin and lactating rats, plasma levels of VP also increased slightly but significantly in response to CCK. During gestation when cardiovascular volume is expanded, both the VP and OT neuroendocrine systems were reset, enabling secretion of both hormones in response to hypovolemia with hypertonicity. During lactation, both neuroendocrine systems are reset such that greater changes in fluid balance are needed to stimulate hormone release. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT, indicative of preferential release of VP with less than a 5% (virgin, pregnant) or a 20% (lactating) loss in blood volume.