AT2R stimulation activates the NO-cGMP-dependent pathway [41] . This occurs either directly or indirectly through bradykinin or by increased endothelial NOS activity or expression. AT2R activation is associated with phosphorylation of JNK, PTPs, IκBα (inhibitor of NF-κB), and the transcription factor ATF2, and dephosphorylation of p38MAPK, ERK1/2, and STAT3, which are linked to antiproliferative and antiinflammatory effects and apoptosis [38, [42] [43] [44] . AT2R may induce relaxation by opening large-conductance Ca 2+ -activated K + channels (BKCa) [45] and by negative regulation of the vascular Rho A/Rho kinase pathway. The AT2R also enhances the activity of tyrosine phosphatases and vanadate-sensitive phosphatases MKP1 (DUSP1), SHP1 (PTPN6) and PP2A [46, 47] .