Aim: 

Recent study demonstrated that the T-type calcium channel (TCC) is expressed in vascular endothelial cells, but their role in endothelial cell function is to be elucidated. We analysed the endothelial functional role of TCC dependent calcium under the Angiotensin II (AngII) stimulation.

Methods: 

The HUVECs were co-incubated with AngII at 10^-7M and either mibefradil 10^-5M (TCC blocker) or Wortmannin 10^-7M (inhibitor of phosphoinositide 3-kinases). The contribution of Ang II receptors is evaluated using PD123319 10^-7M, (AT2 Receptor antagonist) and ZD 7155 10^-7M (AT1 Receptor antagonist). The calcium ion concentration was observed using Fluo-3 acetossimetil (Fluo-3AM). The cells were observed after 3, 6 and 9 hours.

Results: 

The microfluorescence method points out that Ang II increases the [Ca²⁺]_i levels, while the treatments with either wortmannin or mibefradil induces significant decrease of this parameter respectively at short term (3h) and long term (9h). AT2R blockade is necessary to observe significant increase of [Ca²⁺]_i levels. Pretreatment with mibefradil abolishes the Ang II–induced cell migration.

Conclusions: 

Our data show that Ang II, via AT1 receptor increases intracellular calcium levels via IP3, for rapid physiological effects and TCCs pathway for long term effects; the calcium influx via TCCs regulates endothelial cell migration which is essential for angiogenesis.