It is recognized that brain contains all the components of the renin-angiotensin systems (RAS). The nucleus tractus solitarius (NTS) is known to plays a major role in the regulation of cardiovascular, respiratory, gustatory, hepatic and swallowing functions. Voltage- dependent Ca2+ channels (VDCCs) serve as crucial mediators of membrane excitability and Ca2+-dependent functions such as neurotransmitter release, enzyme activity and gene expression. The purpose of this study was to investigate the effects of Angiotensin U (Ang U) on VDCCs currents (ICa) in the NTS using patch-clamp recording methods. An application of Ang U caused facilitation of L-type ICa in a concentration-dependent manner with an EC50 of 167 nM and a Hill coefficient of 1.73. AT1 receptors antagonist, Losartan antagonized the Ang U-induced facilitation of ICa. Intracellular dialysis of the Gi-protein antibody attenuated the Ang U-induced facilitation of ICa. Both Src tyrosine kinase inhibitor and mitogen activated protein kinase (MAPK) inhibitor attenuated the Ang U-induced facilitation of ICa. p38 MAPK inhibitor also attenuated the Ang U- induced facilitation of ICa. These results indicate that Ang U facilitates L-type VDCCs via Gi-proteins involving Src tyrosine kinase and p38 MAPK kinase mediated by AT1 receptors in NTS.