[Mechanism of urotensin II-stimulated adrenomedullin secretion in human vascular endothelial cells]

Di Yi Jun Yi Da Xue Xue Bao. 2005 Jul;25(7):791-3.
[Article in Chinese]

Abstract

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).

Conclusion: Ca(2+), MAPK, CaM-PK and p38 signal transduction pathways may play major roles in U II-stimulated secretion of Adm in HVECs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenomedullin / metabolism*
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Cells, Cultured
  • Endothelial Cells / metabolism*
  • Humans
  • Mitogen-Activated Protein Kinases / metabolism
  • Signal Transduction
  • Urotensins / pharmacology*
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Urotensins
  • Adrenomedullin
  • urotensin II
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases