[Mechanism of urotensin II-stimulated adrenomedullin secretion in human vascular endothelial cells].
OBJECTIVE
To study the mechanism of urotensin II(U II)-stimulated adrenomedullin secretion in human vascular endothelial cells.


METHODS
In cultured human vascular endothelial cells (HEVCs), different concentrations of U II was used to stimulate the secretion of Adm, and different inhibitors were used to study the changes in the secretion after block of different signal transduction pathways. The contents of Adm in the medium were detected with radioimmunoassay.


RESULTS
U II-stimulated Adm secretion in the HEVCs in a time- and concentration-dependent manner. Adm contents of the treatment groups were comparable with that of the control group (P<0.05 ), and the secretion of Adm could be inhibited by the inhibitor of extracellular signal-regulated protein kinases (PD098059), p38 kinase inhibitor (SB202190), calmodulin inhibitor (W7) and Ca(2+) inhibitor (nicardipine)(P<0.05), but calcineurin inhibitor and protein kinase C inhibitor (H7) had no such effect (P>0.05).


CONCLUSIONS
Ca(2+), MAPK, CaM-PK and p38 signal transduction pathways may play major roles in U II-stimulated secretion of Adm in HVECs.
Shi
Xiang-dong
XD
Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Li
Zhi-liang
ZL
Wu
Hong-chao
HC
Wang
Tong-han
TH
Fu
Qiang
Q
Yan
Quan-neng
QN
Tang
Chao-shu
CS
D053607:Adrenomedullin / Q000378:metabolism*; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism*; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D015398:Signal Transduction; D014579:Urotensins / Q000494:pharmacology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D014579:Urotensins; D053607:Adrenomedullin; C029677:urotensin II; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases