1.Study on lipopolysaccharide-stimulated endothelin and adrenomedullin secretion from human vascular endothelial cells and its mechanism
Jingjiong CHEN ; Yongsheng GONG ; Yaqin XU ; Song XU ; Sanbao CHAI ; Yongzheng PANG ; Chaosh TANG
Chinese Journal of Pathophysiology 1989;0(05):-
AIM: To study lipopolysaccharide (LPS)-stimulated secretion of endothelin-1 (ET-1) and adrenomedullin (Adm) from human vascular endothelial cells (HVEC) and its mechanism. METHODS: In cultured HVEC, LPS was used to stimulate ET-1 and Adm secretion from HVEC. The contents of ET-1 and Adm in medium were determined by radioimmunoassay. RESULTS: LPS stimulated secretion of ET-1 and Adm from HVEC in time-dependent and concentration-dependent manner. The ratio of secreted ET-1 to Adm was not changed compared with the control group. The increase of ET-1 could be inhibited by inhibitor of extracellular signal-regulated protein kinases (PD 098059 ) and inhibitor of P38 kinase (SB 202190 )( P 0.05).CONCLUSION: ERKs and P38 signal pathways may play an important role in the secretion of ET-1 from LPS -stimulated HVEC, while only P38 kinase signal pathway is invovled in the secretion of Adm.
2.Study on lipopolysaccharide-stimulated endothelin and adrenomedullin secretion from human vascular endothelial cells and its mechanism
Jingjiong CHEN ; Yongsheng GONG ; Yaqin XU ; Song XU ; Sanbao CHAI ; Yongzheng PANG ; Chaoshu TANG
Chinese Journal of Pathophysiology 2001;17(5):403-406
AIM:To study lipopolysaccharide (LPS)-stimulated secretion of endothelin-1 (ET-1) and adrenomedullin (Adm) from human vascular endothelial cells (HVEC) and its mechanism. METHODS:In cultured HVEC, LPS was used to stimulate ET-1 and Adm secretion from HVEC. The contents of ET-1 and Adm in medium were determined by radioimmunoassay. RESULTS:LPS stimulated secretion of ET-1 and Adm from HVEC in time-dependent and concentration-dependent manner. The ratio of secreted ET-1 to Adm was not changed compared with the control group. The increase of ET-1 could be inhibited by inhibitor of extracellular signal-regulated protein kinases (PD098059) and inhibitor of P38 kinase (SB202190)(P<0.01), while the increase of Adm could only be inhibited by SB202190(P<0.05), both had no response to inhibitor of protein kinase C (H7), inhibitor of calmodulin (W7), inhibitor of calcineurin (cyclosporin A) and inhibitor of Ca2+ (nicardipine)(P>0.05).CONCLUSION:ERKs and P38 signal pathways may play an important role in the secretion of ET-1 from LPS -stimulated HVEC, while only P38 kinase signal pathway is invovled in the secretion of Adm.
3.Effect of chronic hypoxia on L-Arginine/nitric oxide pathway in rat pulmonary artery
Jingjiong CHEN ; Yongsheng GONG ; Luzhen ZHEN ; Zhongsun JIANG ; Chaoshu TANG ; Yongzhen PANG
Chinese Journal of Pathophysiology 1999;0(09):-
AIM: To study the effect of chronic hypoxia on L-Arginine/NO pathway in rat pulmonary artery. METHODS: Changes in pulmonary artery L-Arginine(L-Arg) transport, nitric oxide synthase (NOS) activity, plasma nitrite level and L-Arg level in HPH rats were investigated. RESULTS: (1) The mean pulmonary arterial pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) of HPH group were higher than those in control group (P