The role of nitric oxide in prostaglandin production by human pulmonary artery smooth muscle and endothelial cells.

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Human pulmonary artery smooth muscle cells (HPASMC) were isolated and cultured from autopsy materials, and the effect of sodium nitroprusside (SNP) on cytokine- or lipopolysaccharide (LPS)-induced PGI2 production and expression of COX-2 antigen by HPASMC were examined to elucidate the relationship of the production of NO and prostaglandins by HPASMC. Eicosanoid profile by LPS-stimulated human umbilical vein endothelial ceUs(HUVEC) was also examined by HPLC.1) The enhanced production of PGI2 by LPS- and IL-1β-treated HPASMC was further augmented when HPASMC were treated with LPS or EL-1βtogether with SNP.2) In HUVEC, LPS enhanced the production of cyclooxygenase derivatives, but did not clearly enhance the production of lipoxygenase products. In contrasts, LPS enhanced the production of both cyclooxygenae and lipoxygenase products in HPASMC.3) Western blot analysis revealed that IL-1βaugmented the expression of COX-2 protein in HPASMC,From these experimental findings, it is suggested that1) NO enhances PGI2 production by HPASMC through the increased expression of COX-2 antigen.2) Pulmonary artery smooth muscle cells as well as endothelial cells could actively participate in the regulation of pulmonary blood flow and tonus of pulmonary artery by the interaction of NO and prostaglandins.