一氧化碳抑制人肺动脉平滑肌细胞释放内皮素-1。
Carbon monoxide inhibits endothelin-1 release by human pulmonary artery smooth muscle cells.
作者信息
Stanford Salome J, Walters Matthew J, Mitchell Jane A
机构信息
Unit of Critical Care, The Royal Brompton and Harefield NHS Trust, Imperial College School of Medicine, Sydney Street, London SW3 6NP, UK.
出版信息
Eur J Pharmacol. 2004 Feb 23;486(3):349-52. doi: 10.1016/j.ejphar.2003.12.026.
Endothelin-1 is a potent vasoconstrictor with mitogenic properties. This 21-amino-acid protein, released in the vasculature by endothelial and smooth muscle cells, has been implicated in pulmonary hypertension. More recently, evidence has accumulated for a role of the heme oxygenase system in pulmonary hypertension. Heme oxygenase catalyses the breakdown of heme to produce carbon monoxide, biliverdin and free iron. Here we show that a carbon monoxide-releasing molecule, but not biliverdin, inhibits endothelin-1 release from serum-stimulated human pulmonary artery smooth muscle cells. Under certain conditions, carbon monoxide appears to act as an endogenous break on endothelin-1 release.
内皮素-1是一种具有促有丝分裂特性的强效血管收缩剂。这种由内皮细胞和平滑肌细胞在血管系统中释放的21个氨基酸的蛋白质，与肺动脉高压有关。最近，有越来越多的证据表明血红素加氧酶系统在肺动脉高压中发挥作用。血红素加氧酶催化血红素分解产生一氧化碳、胆绿素和游离铁。在这里，我们表明，一种一氧化碳释放分子而非胆绿素，可抑制血清刺激的人肺动脉平滑肌细胞释放内皮素-1。在某些情况下，一氧化碳似乎作为内皮素-1释放的内源性抑制剂发挥作用。
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