Saluisn-β contributes to endothelial dysfunction in monocrotaline-induced pulmonary arterial hypertensive rats

• DOI: 10.1016/j.biopha.2022.113748
• Publication Date: 2022-09-26T23:04:26Z
• Authors: Yan Pan; Aidong Chen; Xingxing Wang; Changlei Bao; Shuxin Liang; Haiyang Tang; Ying Han
• Keywords: Apocynin; Endothelial Dysfunction; Right ventricular hypertrophy; NAD(P)H oxidase

The endothelial dysfunction and the consequent attenuated pulmonary vasodilatation are major causes of elevated arterial resistance pressure in hypertension (PAH). Current study aimed to explore effects a TOR2A gene product, salusin-β, on endothelium-dependent vascular relaxation progression PAH monocrotaline (MCT)-induced rats as well relevant signaling pathway.Acetylcholine (ACh)-induced dose-dependent was used evaluate function.The salusin-β level plasma artery (PA) MCT-PAH were significantly increased, while ACh-induced attenuated. After incubation or overexpression gene, further deteriorated, anti-salusin-β IgG knockdown improved it rats. superoxide anions scavenger NAC antioxidant apocynin inhibited effect SOD inhibitor DETC enhanced it. nitric oxide (NO) synthase L-NAME almost blocked IgG. Silencing decreased right ventricular (RV) systolic pressure, RV hypertrophy index, NAD(P)H oxidase activity ROS level, increased eNOS NO PA. Overexpression played opposite roles.The saluisn-β plays important roles reduction participates through stimulating oxidase-ROS production inhibiting eNOS-NO release.