The final, formatted version of the article will be published soon.
REVIEW article
Front. Cardiovasc. Med.
Sec. Hypertension
Volume 11 - 2024 |
doi: 10.3389/fcvm.2024.1436059
A neural perspective on the treatment of hypertension: the neurological network excitation and inhibition (E/I) imbalance in Hypertension
Provisionally accepted- 1 Department of anesthesiology, General Hospital of The Yangtze River Shipping, Wuhan Brain Hospital, Wuhan, Hubei Province, China
- 2 Liaoning Provincial Key Laboratory of Cerebral Diseases, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning Province, China
- 3 Emergency Intensive Care Unit, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai, China
- 4 Dalian Medical University, Dalian, China
Despite the increasing number of anti-hypertensive drugs have been developed and used in the clinical setting, persistent deficiencies persist, including issues such as lifelong dosage, combination therapy. Notwithstanding receiving the treatment under enduring these deficiencies, approximately 4 in 5 patients still fail to achieve reliable blood pressure (BP) control. The application of neuromodulation in the context of hypertension presents a pioneering strategy for addressing this condition, con-currently implying a potential central nervous mechanism underlying hypertension onset. We hypothesize that neurological networks, an essential component of maintaining appropriate neurological function, are involved in hypertension. Drawing on both peer-reviewed research and our laboratory investigations, we endeavor to investigate the underlying neural mechanisms involved in hypertension by identifying a close relationship between its onset of hypertension and an excitation and inhibition (E/I) imbalance. In addition to the involvement of excitatory glutamatergic and GABAergic inhibitory system, the pathogenesis of hypertension is also associated with Voltagegated sodium channels (VGSCs, Nav)-mediated E/I balance. The overloading of glutamate or enhancement of glutamate receptors may be attributed to the E/I imbalance, ultimately triggering hypertension. GABA loss and GABA receptor dysfunction have also proven to be involved. Furthermore, we have identified that abnormalities in sodium channel expression and function alter neural excitability, thereby disturbing E/I balance and potentially serving as a mechanism underlying hypertension. These insights are expected to furnish potential strategies for the advancement of innovative anti-hypertensive therapies and a meaningful reference for the exploration of central nervous system (CNS) targets of anti-hypertensives.
Keywords: Hypertension, Neural Network, E/I imbalance, Neural connection, sympathetic outflow
Received: 21 May 2024; Accepted: 29 Aug 2024.
Copyright: © 2024 Xia, Wang, Wang, Hu, Chen and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Tianyu Wang, Liaoning Provincial Key Laboratory of Cerebral Diseases, College of Basic Medical Sciences, Dalian Medical University, Dalian, 116044, Liaoning Province, China
Tingting Hu, Department of anesthesiology, General Hospital of The Yangtze River Shipping, Wuhan Brain Hospital, Wuhan, Hubei Province, China
Defang Chen, Emergency Intensive Care Unit, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai, China
Bin Wang, Dalian Medical University, Dalian, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.