High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons.

High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons.
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DOI:
10.1016/j.celrep.2021.108866
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发表时间:
2021-03-16
期刊:
影响因子:
8.8
通讯作者:
Bourque CW
Bourque CW
中科院分区:
生物学1区
文献类型:
--
作者:
Levi DI;Wyrosdic JC;Hicks AI;Andrade MA;Toney GM;Prager-Khoutorsky M;Bourque CW

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高盐饮食增加动脉压,部分是通过激活大细胞神经分泌细胞(MNCVP)分泌抗利尿和血管收缩激素血管加压素(VP)进入循环。在这里,我们表明,由高渗引起的MNCVP的内在和突触兴奋差异增强两种模型的盐依赖性高血压大鼠。一个模型将高盐食物与慢性降压剂量的血管紧张素II(AngII-盐)相结合,另一个模型涉及用2%NaCl(盐负荷,SL)代替饮用水。在这两种模型中,我们观察到的量子振幅的EPSC MNCVP显着增加。然而,也观察到了模型特定的变化。血管紧张素II-盐增加谷氨酸释放的可能性,通过β受体传入和增加整体兴奋性网络驱动。与此相反,SL专门增加膜刚度和固有的MNCVP的抗氧化剂的敏感性。这些结果表明,膳食盐通过影响MNCVP的细胞自主性和突触的兴奋性增加MNCVP。Levi等人表明,大鼠经历了两种不同的盐依赖性高血压模型,其特征是神经分泌神经元的神经反应性增加,这些神经分泌神经元释放抗利尿和血管收缩激素加压素。然而,这种共同的效应与表征每个模型的不同细胞和突触变化相关。
High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells (MNCVP) that secrete the antidiuretic and vasoconstrictor hormone vasopressin (VP) into the circulation. Here, we show that the intrinsic and synaptic excitation of MNCVP caused by hypertonicity are differentially potentiated in two models of salt-dependent hypertension in rats. One model combined salty chow with a chronic subpressor dose of angiotensin II (AngII-salt), the other involved replacing drinking water with 2% NaCl (salt loading, SL). In both models, we observed a significant increase in the quantal amplitude of EPSCs on MNCVP. However, model-specific changes were also observed. AngII-salt increased the probability of glutamate release by osmoreceptor afferents and increased overall excitatory network drive. In contrast, SL specifically increased membrane stiffness and the intrinsic osmosensitivity of MNCVP. These results reveal that dietary salt increases the excitability of MNCVP through effects on the cell-autonomous and synaptic osmoresponsiveness of MNCVP. Levi et al. show that rats subjected to two distinct models of salt-dependent hypertension feature an increase in the osmoresponsiveness of neurosecretory neurons that release the antidiuretic and vasoconstrictor hormone vasopressin. However, this common effect is associated with different cellular and synaptic changes that characterize each of the models.
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