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.