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Pharmacological inhibition of the F -ATPase/P2Y pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation.

Acta Physiol (Oxf). 2019; 
CabouCendrine,HonoratoPaula,BriceñoLuis,GhezaliLamia,DuparcThibaut,LeónMarcelo,CombesGuillaume,FrayssinhesLaure,FournelAudren,AbotAnne,MasriBernard,ParadaNicol,AguileraValeria,AguayoClaudio,KnaufClaude,GonzálezMarcelo,RadojkovicClaudia,MartinezLaure
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摘要

The contribution of apolipoprotein A1 (APOA1), the major apolipoprotein of high-density lipoprotein (HDL), to endothelium-dependent vasodilatation is unclear, and there is little information regarding endothelial receptors involved in this effect. Ecto-F -ATPase is a receptor for APOA1, and its activity in endothelial cells is coupled to adenosine diphosphate (ADP)-sensitive P2Y receptors (P2Y ADP receptors). Ecto-F -ATPase is involved in APOA1-mediated cell proliferation and HDL transcytosis. Here, we investigated the effect of lipid-free APOA1 and the involvement of ecto-F -ATPase and P2Y ADP receptors on nitric oxide (NO) synthesis and the regulation of vascular tone.

关键词

F1-ATPase,apolipoprotein A1,endothelial cells,nitric oxide,purinergic recep