Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, SD 57069, Vermillion, USA.
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.
Curr Hypertens Rep. 2022 Jul;24(7):235-246. doi: 10.1007/s11906-022-01187-4. Epub 2022 Apr 6.
This review focuses on studies implicating forebrain neural pathways and neuromodulator systems, particularly, the nitric oxide system within the paraventricular nucleus of the hypothalamus in regulating neurohumoral drive, autonomic pathways, and fluid balance.
Accumulating evidence from animals with experimental models of hypertension and heart failure as well as humans with hypertension suggests that alterations in central neural pathways, particularly, within the PVN neuromodulated by neuronal nitric oxide, are involved in regulating sympathetic outflow particularly to the kidney resulting in alterations in fluid balance commonly observed in hypertension and heart failure states. The characteristics of the hypertensive and heart failure states include alterations in neuronal nitric oxide within the PVN to cause an increase in renal sympathetic nerve activity to result in sodium and fluid retention in these diseases. A comprehensive understanding of these mechanisms will enhance our ability to treat hypertensive and heart failure conditions and their cardiovascular complications more efficiently.
本综述重点介绍了涉及脑前神经通路和神经调质系统，特别是下丘脑室旁核一氧化氮系统，在调节神经激素驱动、自主通路和液体平衡中的作用的研究。
来自高血压和心力衰竭动物实验模型以及高血压人类的累积证据表明，中枢神经通路的改变，特别是神经元一氧化氮调制的室旁核内的神经通路的改变，参与调节交感传出，特别是对肾脏的传出，导致在高血压和心力衰竭状态中常见的液体平衡改变。高血压和心力衰竭状态的特征包括室旁核内神经元一氧化氮的改变，导致肾交感神经活动增加，从而导致这些疾病中的钠和液体潴留。对这些机制的全面理解将提高我们更有效地治疗高血压和心力衰竭及其心血管并发症的能力。
