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在戈德布拉特高血压模型中,下丘脑室旁核可不同程度地诱发交感缩血管活动的频率编码模式。

Frequency-coded patterns of sympathetic vasomotor activity are differentially evoked by the paraventricular nucleus of the hypothalamus in the Goldblatt hypertension model.

作者信息

Faber Jean, Milanez Maycon I O, Simões Cristiano S, Campos Ruy R

机构信息

Neuroscience Division, Department of Neurology and Neurosurgery, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.

Cardiovascular Division, Department of Physiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.

出版信息

Front Cell Neurosci. 2023 Aug 22;17:1176634. doi: 10.3389/fncel.2023.1176634. eCollection 2023.

DOI:10.3389/fncel.2023.1176634
PMID:37674868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10477436/
Abstract

INTRODUCTION

The paraventricular nucleus of the hypothalamus (PVN) contains premotor neurons involved in the control of sympathetic vasomotor activity. It is known that the stimulation of specific areas of the PVN can lead to distinct response patterns at different target territories. The underlying mechanisms, however, are still unclear. Recent evidence from sympathetic nerve recording suggests that relevant information is coded in the power distribution of the signal along the frequency range. In the present study, we addressed the hypothesis that the PVN is capable of organizing specific spectral patterns of sympathetic vasomotor activation to distinct territories in both normal and hypertensive animals.

METHODS

To test it, we investigated the territorially differential changes in the frequency parameters of the renal and splanchnic sympathetic nerve activity (rSNA and sSNA, respectively), before and after disinhibition of the PVN by bicuculline microinjection. Subjects were control and Goldblatt rats, a sympathetic overactivity-characterized model of neurogenic hypertension (2K1C). Additionally, considering the importance of angiotensin II type 1 receptors (AT1) in the sympathetic responses triggered by bicuculline in the PVN, we also investigated the impact of angiotensin AT1 receptors blockade in the spectral features of the rSNA and sSNA activity.

RESULTS

The results revealed that each nerve activity (renal and splanchnic) presents its own electrophysiological pattern of frequency-coded rhythm in each group (control, 2K1C, and 2K1C treated with AT1 antagonist losartan) in basal condition and after bicuculline microinjection, but with no significant differences regarding total power comparison among groups. Additionally, the losartan 2K1C treated group showed no decrease in the hypertensive response triggered by bicuculline when compared to the non-treated 2K1C group. However, their spectral patterns of sympathetic nerve activity were different from the other two groups (control and 2K1C), suggesting that the blockade of AT1 receptors does not totally recover the basal levels of neither the autonomic responses nor the electrophysiological patterns in Goldblatt rats, but act on their spectral frequency distribution.

DISCUSSION

The results suggest that the differential responses evoked by the PVN were preferentially coded in frequency, but not in the global power of the vasomotor sympathetic responses, indicating that the PVN is able to independently control the frequency and the power of sympathetic discharges to different territories.

摘要

引言

下丘脑室旁核(PVN)包含参与控制交感血管运动活动的运动前神经元。已知刺激PVN的特定区域可导致在不同靶区域产生不同的反应模式。然而,其潜在机制仍不清楚。来自交感神经记录的最新证据表明,相关信息编码在信号沿频率范围的功率分布中。在本研究中,我们探讨了以下假设:在正常和高血压动物中,PVN能够组织交感血管运动激活到不同区域的特定频谱模式。

方法

为了验证这一假设,我们通过微量注射荷包牡丹碱解除PVN抑制之前和之后,研究了肾交感神经活动和内脏交感神经活动(分别为rSNA和sSNA)频率参数的区域差异变化。实验对象为对照大鼠和戈德布拉特大鼠,后者是一种以交感神经过度活跃为特征的神经源性高血压模型(2K1C)。此外,考虑到1型血管紧张素II受体(AT1)在PVN中荷包牡丹碱触发的交感反应中的重要性,我们还研究了血管紧张素AT1受体阻断对rSNA和sSNA活动频谱特征的影响。

结果

结果显示,在基础状态和微量注射荷包牡丹碱后,每组(对照、2K1C以及用AT1拮抗剂氯沙坦治疗的2K1C)的每种神经活动(肾和内脏)均呈现其自身的频率编码节律的电生理模式,但各组之间在总功率比较方面无显著差异。此外,与未治疗的2K1C组相比,用氯沙坦治疗的2K1C组在荷包牡丹碱触发的高血压反应方面没有降低。然而,它们的交感神经活动频谱模式与其他两组(对照和2K1C)不同,这表明阻断AT1受体并不能完全恢复戈德布拉特大鼠自主反应的基础水平或电生理模式,而是作用于其频谱频率分布。

讨论

结果表明,PVN诱发的差异反应优先以频率编码,而非血管运动交感反应的整体功率,这表明PVN能够独立控制向不同区域的交感神经放电的频率和功率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/9994f9b4976a/fncel-17-1176634-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/9251b1b7f65f/fncel-17-1176634-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/6a982c178aae/fncel-17-1176634-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/6a417816bb22/fncel-17-1176634-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/9994f9b4976a/fncel-17-1176634-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/9251b1b7f65f/fncel-17-1176634-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/6a982c178aae/fncel-17-1176634-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/6a417816bb22/fncel-17-1176634-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebda/10477436/9994f9b4976a/fncel-17-1176634-g004.jpg

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