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Current Neurovascular Research

Editor-in-Chief

ISSN (Print): 1567-2026
ISSN (Online): 1875-5739

Review Article

Clinical Significance of the Sympathetic Nervous System in the Development and Progression of Pulmonary Arterial Hypertension

Author(s): Ru-Xia Liu, Qian Luo, Hui Qiao, Juan Yu, Qian-Long Zhang, Peng Wang, Yong-Gang Cao, Chang-Lin Jiang and Li-Hui Qu*

Volume 14, Issue 2, 2017

Page: [190 - 198] Pages: 9

DOI: 10.2174/1567202614666170112165927

Price: $65

Abstract

Background: Pulmonary arterial hypertension (PAH) is defined as a complex disease of clinically characterized by elevated pulmonary pressure eventually resulting in right heart failure and premature death. To date, PAH still remains a life-threatening disease. Published evidence suggests that patients with PAH present profound sympathetic nervous system abnormalities and sympathetic activity has been shown to be increased. The mechanism of PAH is still complex and poorly understood.

Results: Some data have showed that adrenoceptors are involved in the process of the pathology and have different functions in the progression of PAH followed by heart failure. Alpha-adrenergic receptors mediate most excitatory effects and induce growth of smooth muscle cells and adventitial fibroblasts via complex cellular and molecular mechanisms. However, beta-adrenergic receptor mainly detected in endothelial layer commonly exerts relaxation effects on pulmonary artery. In addition, G protein-coupled receptor kinase 2, the primary G protein-coupled receptor kinase expressed in the heart, has been shown to be increased, resulting in the distinctive loss of inotropic reserve and functional capacity of the failing heart according to the activation of sympathetic nervous system.

Conclusion: Here, we summarize the relevant available studies describing the roles of sympathetic nervous system in the progression of PAH.

Keywords: Pulmonary arterial hypertension, sympathetic nervous system, adrenergic signaling, vascular remodeling, G protein-coupled receptor kinase 2, heart failure.


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