title: Clinical Significance of the Sympathetic Nervous System in the Development and Progression of Pulmonary Arterial Hypertension.
abstract: 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.
  
  
  
  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.
  
  
  
  Here, we summarize the relevant available studies describing the roles of sympathetic nervous system in the progression of PAH.
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Ru-Xia
authors.initials: RX
authors.lastname: Liu
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Luo
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Qiao
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Yu
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Qian-Long
authors.initials: QL
authors.lastname: Zhang
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.affiliation: Department of Pharmacology, College of Basic Medical Sciences, Harbin Medical University-Daqing, Daqing, China.
authors.forename: Yong-Gang
authors.initials: YG
authors.lastname: Cao
authors.affiliation: Department of Pain, Daqing Oilfield General Hospital, Daqing, China.
authors.forename: Chang-Lin
authors.initials: CL
authors.lastname: Jiang
authors.affiliation: Department of Physiology, College of Basic Medical Sciences, Harbin Medical University-Daqing, 39 Xinyang Rd., Gaoxin District, Daqing, Heilongjiang 163319, China.
authors.forename: Li-Hui
authors.initials: LH
authors.lastname: Qu
mesh_terms: D018450:Disease Progression; D054768:G-Protein-Coupled Receptor Kinases / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications / Q000473:pathology*; D008297:Male; D011941:Receptors, Adrenergic / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D011941:Receptors, Adrenergic; D054768:G-Protein-Coupled Receptor Kinases
keywords: G
  protein-coupled receptor kinase 2; Pulmonary arterial hypertension; adrenergic signaling; heart failure; sympathetic nervous system; vascular remodeling