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Sodium pumps, ouabain and aldosterone in the brain: A neuromodulatory pathway underlying salt-sensitive hypertension and heart failure.
Cell Calcium ( IF 4.3 ) Pub Date : 2019-12-17 , DOI: 10.1016/j.ceca.2019.102151 Frans H H Leenen 1 , Hong-Wei Wang 1 , John M Hamlyn 2
Cell Calcium ( IF 4.3 ) Pub Date : 2019-12-17 , DOI: 10.1016/j.ceca.2019.102151 Frans H H Leenen 1 , Hong-Wei Wang 1 , John M Hamlyn 2
Affiliation
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Accumulating evidence obtained over the last three decades has revealed a neuroendocrine system in the brain that mediates long term increases in blood pressure. The system involves distinct ion transport pathways including the alpha-2 isoform of the Na,K pump and epithelial sodium channels, as well as critical hormone elements such as angiotensin II, aldosterone, mineralocorticoid receptors and endogenous ouabain. Activation of this system either by circulating or central sodium ions and/or angiotensin II leads to a cascading sequence of events that begins in the hypothalamus and involves the participation of several brain nuclei including the subfornical organ, supraoptic and paraventricular nuclei and the rostral ventral medulla. Key events include heightened aldosterone synthesis and mineralocorticoid receptor activation, upregulation of epithelial sodium channels, augmented synthesis and secretion of endogenous ouabain from hypothalamic magnocellular neurons, and sustained increases in sympathetic outflow. The latter step depends upon increased production of angiotensin II and the primary amplification of angiotensin II type I receptor signaling from the paraventricular nucleus to the rostral ventral lateral medulla. The transmission of sympathetic traffic is secondarily amplified in the periphery by increased short- and long-term potentiation in sympathetic ganglia and by sustained actions of endogenous ouabain in the vascular wall that augment expression of sodium calcium exchange, increase cytosolic Ca2+ and heighten myogenic tone and contractility. Upregulation of this multi-amplifier system participates in forms of hypertension where salt, angiotensin and/or aldosterone are elevated and contributes to adverse outcomes in heart failure.
中文翻译：
脑中的钠泵，哇巴因和醛固酮：盐敏感性高血压和心力衰竭的神经调节途径。
在过去的三十年中，越来越多的证据表明，大脑中的神经内分泌系统可调节血压的长期升高。该系统涉及独特的离子传输途径，包括Na，K泵的α-2亚型和上皮钠通道，以及关键的激素元素，例如血管紧张素II，醛固酮，盐皮质激素受体和内源性哇巴因。通过循环或中央钠离子和/或血管紧张素II激活该系统会导致一系列事件的级联序列，该事件始于下丘脑，并涉及多个大脑核的参与，包括子房下器官，视上和脑室旁核以及延髓腹侧延髓。关键事件包括醛固酮合成增加和盐皮质激素受体活化，上皮钠通道的上调，下丘脑大细胞神经元内源性哇巴因的合成和分泌增加以及交感神经外流持续增加。后面的步骤取决于增加的血管紧张素II产生和血管紧张素II型I受体信号从心室旁核到延髓腹侧外侧延髓的初步扩增。其次，交感神经节的短期和长期增强作用以及血管壁内源性哇巴因的持续作用增加了钠钙交换的表达，增加了胞浆中的Ca2 +并增强了肌原性调和，从而增加了交感神经传递的传播。收缩力。这种多功放系统的上调会导致高血压，其中盐分，
更新日期：2019-12-18
中文翻译：
脑中的钠泵，哇巴因和醛固酮：盐敏感性高血压和心力衰竭的神经调节途径。
在过去的三十年中，越来越多的证据表明，大脑中的神经内分泌系统可调节血压的长期升高。该系统涉及独特的离子传输途径，包括Na，K泵的α-2亚型和上皮钠通道，以及关键的激素元素，例如血管紧张素II，醛固酮，盐皮质激素受体和内源性哇巴因。通过循环或中央钠离子和/或血管紧张素II激活该系统会导致一系列事件的级联序列，该事件始于下丘脑，并涉及多个大脑核的参与，包括子房下器官，视上和脑室旁核以及延髓腹侧延髓。关键事件包括醛固酮合成增加和盐皮质激素受体活化，上皮钠通道的上调，下丘脑大细胞神经元内源性哇巴因的合成和分泌增加以及交感神经外流持续增加。后面的步骤取决于增加的血管紧张素II产生和血管紧张素II型I受体信号从心室旁核到延髓腹侧外侧延髓的初步扩增。其次，交感神经节的短期和长期增强作用以及血管壁内源性哇巴因的持续作用增加了钠钙交换的表达，增加了胞浆中的Ca2 +并增强了肌原性调和，从而增加了交感神经传递的传播。收缩力。这种多功放系统的上调会导致高血压，其中盐分，
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