title: [Nitric oxide and endothelins in pulmonary hypertension].
abstract: For recent decades, the medical treatment of primary pulmonary hypertension(PH) have shown an improved outcome as a bridge to lung transplantation. Both nitric oxide (NO) and endothelin(ET) have reported as a major vasoactive mediators in initiating PH. NO is a potent vasodilator released from endothelial cells to adjacent smooth muscle cells in vascular wall. Inhalation of NO has exerted dramatic effects with minimum complication for PH patients. ET-1, after binding to ETA receptor, promotes a strong vasoconstriction, cell growth and platelet aggregation. ETB receptor promotes the clearance of circulating ET-1 in the lung, and stimulates the release of NO and PGI2. Therapeutic trials of ETA receptor antagonist and NO donors for PH may be promising because of their direct action against vasoconstriction.
authors: Department of Pediatrics, Toho University, Sakura Hospital.
authors: Y
authors: Y
authors: Aoki
authors: T
authors: T
authors: Saji
mesh_terms: D065128:Endothelin Receptor Antagonists; D016232:Endothelins / Q000502:physiology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology*; D009569:Nitric Oxide / Q000502:physiology* / Q000627:therapeutic use; D020033:Protein Isoforms / Q000502:physiology; D017466:Receptors, Endothelin / Q000502:physiology
chemical_list: D065128:Endothelin Receptor Antagonists; D016232:Endothelins; D020033:Protein Isoforms; D017466:Receptors, Endothelin; D009569:Nitric Oxide