Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats.
Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats.
复制标题
慢性孤束核损伤不会阻止大鼠低血容量诱导的加压素分泌。
DOI：
10.1152/ajpregu.1994.267.4.r965
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Sved,AF
中科院分区：
文献类型：
--
作者：
Schreihofer,AM;Stricker,EM;Sved,AF
本研究验证了低血容量通过消除紧张性抑制性压力感受器输入刺激血管加压素（VP）分泌的假说。连续出血（每10分钟取4份2 ml/300 g体重的样本）增加了清醒大鼠的血浆VP水平，这些大鼠由于慢性双侧孤束核（NTS）损伤而缺乏心脏和动脉压力感受器反射反应。VP对出血的反应与对照组大鼠和慢性去窦房结神经（SAD）大鼠相似。皮下注射30%聚乙二醇后，NTS损伤大鼠、SAD大鼠和对照大鼠的VP水平升高，这与诱导的血浆容量减少相关。此外，在α-氯醛糖麻醉的对照大鼠，慢性SAD大鼠和慢性NTS损伤大鼠，双侧迷走神经切断术对基础VP水平的影响很小，慢性NTS损伤大鼠迷走神经切断术并不能阻止血管紧张素诱发的VP分泌增加。这些结果并不支持这样的想法，即通过减少紧张性抑制压力感受器输入，血管紧张素诱导的VP分泌。相反，无论是心脏还是动脉压力感受器输入似乎是必要的低血容量诱导的VP分泌大鼠。
The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.