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内脏神经和迷走神经去神经支配减弱大鼠中枢Fos蛋白的表达,但不减弱对胃内盐分的抗利尿激素反应。

Splanchnic and vagal denervation attenuate central Fos but not AVP responses to intragastric salt in rats.

作者信息

Carlson S H, Osborn J W

机构信息

Department of Physiology, University of Minnesota, Saint Paul 55108, USA.

出版信息

Am J Physiol. 1998 May;274(5):R1243-52. doi: 10.1152/ajpregu.1998.274.5.R1243.

Abstract

We have recently reported that an acute intragastric hypertonic saline load increases plasma arginine vasopressin (PAVP) and Fos immunoreactivity in several central nuclei, including the supraoptic nucleus (SON), paraventricular nucleus (PVN), nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (LPBN). We hypothesized that these responses are mediated by stimulation of peripheral osmoreceptors with splanchnic and/or vagal afferent projections. To test this hypothesis, we examined the effect of bilateral subdiaphragmatic vagotomy and bilateral splanchnic denervation on the PAVP and Fos immunoreactivity responses to intragastric hypertonic saline infusion in awake rats. Compared with responses in sham rats, Fos immunoreactivity responses were significantly reduced in vagotomized rats in the AP, SON, and PVN, whereas normal Fos levels were observed in the LPBN. However, vagotomized rats exhibited a normal increase in PAVP. Splanchnic-denervated rats also exhibited similar changes in PAVP in response to intragastric hypertonic saline compared with sham-denervated rats, and no differences were observed in Fos immunoreactivity in the LPBN, SON, and PVN compared with sham rats. However, splanchnic-denervated rats were observed to have significantly lower Fos staining in the NTS and AP compared with sham rats. The inability of splanchnic or vagal denervation alone to block the PAVP response to intragastric hypertonic saline suggests that either peripheral osmoreceptors project via both splanchnic and vagal afferents to mediate AVP release or that the observed response of PAVP is due to the activation of central osmoreceptors in the absence of measurable changes in plasma osmolality.

摘要

我们最近报道,急性胃内高渗盐水负荷可增加多个中枢核团中的血浆精氨酸加压素(PAVP)和Fos免疫反应性,这些核团包括视上核(SON)、室旁核(PVN)、孤束核(NTS)、最后区(AP)和外侧臂旁核(LPBN)。我们推测这些反应是由内脏和/或迷走神经传入投射刺激外周渗透压感受器介导的。为了验证这一假设,我们研究了双侧膈下迷走神经切断术和双侧内脏去神经支配对清醒大鼠胃内输注高渗盐水时PAVP和Fos免疫反应性的影响。与假手术大鼠的反应相比,迷走神经切断术大鼠在AP、SON和PVN中的Fos免疫反应性显著降低,而在LPBN中观察到正常的Fos水平。然而,迷走神经切断术大鼠的PAVP正常升高。与假去神经支配大鼠相比,内脏去神经支配大鼠对胃内高渗盐水的反应中PAVP也有类似变化,并且与假手术大鼠相比,LPBN、SON和PVN中的Fos免疫反应性没有差异。然而,与假手术大鼠相比,观察到内脏去神经支配大鼠在NTS和AP中的Fos染色明显较低。单独的内脏或迷走神经去神经支配不能阻断PAVP对胃内高渗盐水的反应,这表明要么外周渗透压感受器通过内脏和迷走神经传入投射介导AVP释放,要么观察到的PAVP反应是由于在血浆渗透压无明显变化的情况下中枢渗透压感受器的激活。

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