Endothelial C-type natriuretic peptide/guanylyl cyclase-B signaling prevents pulmonary arterial hypertension
This study investigates the significance of endothelial C-type natriuretic peptide (CNP) and its receptor guanylyl cyclase-B (GC-B) in the development of pulmonary arterial hypertension (PAH). The authors demonstrate tha
C-type natriuretic peptide (CNP) is released from endothelial cells and acts as an autocrine/paracrine mediator, regulating systemic blood pressure and vascular remodeling via guanylyl cyclase-B (GC-B) and natriuretic peptide receptor-C. The authors investigate the impact of vascular CNP/GC-B signaling on the development of PAH using multiple models. Mice developing pulmonary hypertension show reduced pulmonary NPPC and NPR2 expression than mice without PH. Similarly, endothelial cells from patients with idiopathic PAH exhibit lower NPPC and NPR2 expression than control EC.