Abstract
ACE2 and Ang1–7 have been shown to protect against pulmonary hypertension (PH). Mechanisms remain unclear. Considering the important role of ET-1 in PH pathophysiology and endothelial dysfunction, we asked whether Ang1–7 influences ET-1 signalling in PH. Human endothelial cells (HMEC) were stimulated with ET-1 in absence/presence of Ang1–7 and showed that Ang1–7 increased ET-1 release (125%) and ETBR protein (50%), p in vitro validation. We previously demonstrated in HMEC that Ang1–7 stimulates Akt phosphorylation (180%), an effect inhibited by peptide disruptors, p
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