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首页> 外文期刊>American Journal of Physiology >Blockade of NK3R signaling in the PVN decreases vasopressin and oxytocin release and c-Fos expression in the magnocellular neurons in response to hypotension.
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Blockade of NK3R signaling in the PVN decreases vasopressin and oxytocin release and c-Fos expression in the magnocellular neurons in response to hypotension.

机译：对PVN的NK3R信号传导的阻滞可降低血管降压素和催产素的释放以及响应低血压的大细胞神经元中c-Fos的表达。

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摘要

Tachykinin neurokinin 3 receptor (NK3R) signaling has a broad role in vasopressin (VP) and oxytocin (OT) release. Hydralazine (HDZ)-induced hypotension activates NK3R expressed by magnocellular neurons, increases plasma VP and OT levels, and induces c-Fos expression in VP and OT neurons. Intraventricular pretreatment with the specific NK3R antagonist, SB-222200, eliminates the HDZ-stimulated VP and OT release. NK3R are distributed in the central pathways conveying hypotension information to the magnocellular neurons, and the NK3R antagonist could act anywhere in the pathways. Alternatively, the antagonist could act at the NK3R expressed by the magnocellular neurons. To determine whether blockade of NK3R on magnocellular neurons impairs VP and OT release to HDZ, rats were pretreated with a unilateral PVN injection of 0.15 M NaCl or SB-222200 prior to an intravenous injection of 0.15 M NaCl or HDZ. Blood samples were taken, and brains were processed for VP/c-Fos and OT/c-Fos immunohistochemistry. Intravenous injection of 0.15 M NaCl did not alter plasma hormone levels, and little c-Fos immunoreactivity was present in the PVN. Conversely, intravenous injection of HDZ increased plasma VP and OT levels and c-Fos expression in VP and OT magnocellular neurons. Intra-PVN injection of SB-222200 prior to an intravenous injection of HDZ significantly decreased c-Fos expression in both VP and OT neurons by approximately 70% and attenuated plasma VP and OT levels by 33% and 35%, respectively. Therefore, NK3R signaling in magnocellular neurons has a critical role for the release of VP and OT in response to hypotension.
机译：速激肽神经激肽3受体（NK3R）信号在血管加压素（VP）和催产素（OT）释放中具有广泛的作用。肼屈嗪（HDZ）引起的低血压激活了巨细胞神经元表达的NK3R，增加了血浆VP和OT水平，并诱导VP和OT神经元中的c-Fos表达。用特定的NK3R拮抗剂SB-222200进行脑室内预处理可消除HDZ刺激的VP和OT释放。 NK3R分布在将低血压信息传递给大细胞神经元的中央通路中，而NK3R拮抗剂可以在通路的任何位置起作用。或者，拮抗剂可以作用于由巨细胞神经元表达的NK3R。为了确定对大细胞神经元的NK3R阻滞是否损害VP和OT向HDZ的释放，在静脉内注射0.15 M NaCl或HDZ之前，先对大鼠进行单侧PVN注射0.15 M NaCl或SB-222200预处理。采集血样，并对大脑进行VP / c-Fos和OT / c-Fos免疫组织化学处理。静脉注射0.15 M NaCl不会改变血浆激素水平，PVN中几乎没有c-Fos免疫反应性。相反，静脉注射HDZ可增加VP和OT巨细胞神经元的血浆VP和OT水平以及c-Fos表达。在静脉注射HDZ之前，对SB-222200进行PVN内注射可显着降低VP和OT神经元中c-Fos的表达约70％，并使血浆VP和OT水平分别降低33％和35％。因此，大细胞神经元中的NK3R信号传导对于响应低血压而释放VP和OT具有至关重要的作用。

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