Angiotensin II regulates endothelial cell migration through calcium influx via T-type calcium channel in the Human Umbilical Vein Endothelial Cells

Aim: The T-type calcium channel is expressed in vascular endothelial cells,but its role in endothelial cell function is yet to be elucidated. We analysedthe endothelial functional role of T-type calcium channel-dependent calciumunder angiotensin II (Ang II) stimulation.Methods: Human umbilical vein endothelial cells were co-incubated withhormone at 10)7 m and either Efonidipine 10)5 m or Verapamil 10)5 m orMibefradil 10)5 m or Wortmannin 10)6 m. The contribution of Ang IIreceptors was evaluated using PD123319 10)7 m and ZD 7155 10)7 m. Thecalcium ion concentration was observed using Fluo-3 acetossimetil ester. Thecells were observed after 3, 6, 9 and 12 h.Results: The microfluorescence method points out that Ang II inducesintracellular calcium modulation in time by distinct mechanisms. AT2receptor blockade is necessary to observe significant increase in [Ca2+]i levels.Pre-treatment with Mibefradil abolishes Ang II -induced cell migration.Conclusions: Our data show that Ang II, via AT1 receptor, modulatescalcium concentration involving T-type calcium channel and L-type calciumchannel but only the calcium influx via T-type calcium channels regulatesendothelial cell migration which is essential for angiogenesis.Keywords angiotensin II, HUVEC, mibefradil, verapamil, voltageoperatedcalcium channels.