Department of Physiology and Functional Genomics, University of Florida, College of Medicine, 1345 Center Drive, Gainesville, FL 32610, USA.
Curr Hypertens Rep. 2013 Aug;15(4):377-89. doi: 10.1007/s11906-013-0361-4.
It is widely accepted that the pathophysiology of hypertension involves autonomic nervous system dysfunction, as well as a multitude of immune responses. However, the close interplay of these systems in the development and establishment of high blood pressure and its associated pathophysiology remains elusive and is the subject of extensive investigation. It has been proposed that an imbalance of the neuro-immune systems is a result of an enhancement of the "proinflammatory sympathetic" arm in conjunction with dampening of the "anti-inflammatory parasympathetic" arm of the autonomic nervous system. In addition to the neuronal modulation of the immune system, it is proposed that key inflammatory responses are relayed back to the central nervous system and alter the neuronal communication to the periphery. The overall objective of this review is to critically discuss recent advances in the understanding of autonomic immune modulation, and propose a unifying hypothesis underlying the mechanisms leading to the development and maintenance of hypertension, with particular emphasis on the bone marrow, as it is a crucial meeting point for neural, immune, and vascular networks.
人们普遍认为，高血压的病理生理学涉及自主神经系统功能障碍以及多种免疫反应。然而，这些系统在高血压的发展和确立及其相关病理生理学中的紧密相互作用仍然难以捉摸，这也是广泛研究的主题。有人提出，神经-免疫系统的失衡是由于“促炎交感神经”臂的增强以及自主神经系统的“抗炎副交感神经”臂的抑制所致。除了神经元对免疫系统的调节外，还提出关键的炎症反应会被传递回中枢神经系统，并改变神经元对外周的通讯。本综述的总体目标是批判性地讨论自主免疫调节的最新进展，并提出一个统一的假说，该假说阐明了导致高血压发展和维持的机制，特别强调骨髓，因为骨髓是神经、免疫和血管网络的关键交汇点。
