In human umbilical vein endothelial cells, Angiotensin II regulates cell migration essential for angiogenesis specifically through calcium influx via T-type calcium channels.
T-type Ca channel blockade may blunt Ang II-driven endothelial migration; leaves open in vivo validation and clinical translation.
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 analysed the endothelial functional role of T-type calcium channel-dependent calcium under angiotensin II (Ang II) stimulation. METHODS: Human umbilical vein endothelial cells were co-incubated with hormone at 10(-7) m and either Efonidipine 10(-5) m or Verapamil 10(-5) m or Mibefradil 10(-5) m or Wortmannin 10(-6) m. The contribution of Ang II receptors was evaluated using PD123319 10(-7) m and ZD 7155 10(-7) m. The calcium ion concentration was observed using Fluo-3 acetossimetil ester. The cells were observed after 3, 6, 9 and 12 h. RESULTS: The microfluorescence method points out that Ang II induces intracellular calcium modulation in time by distinct mechanisms. AT2 receptor blockade is necessary to observe significant increase in [Ca(2+)](i) levels. Pre-treatment with Mibefradil abolishes Ang II -induced cell migration. CONCLUSIONS: Our data show that Ang II, via AT1 receptor, modulates calcium concentration involving T-type calcium channel and L-type calcium channel but only the calcium influx via T-type calcium channels regulates endothelial cell migration which is essential for angiogenesis.
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Martini et al. (2009) studied this question.
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