AGT and ischemia: Supported by experimental evidence [3,4], several neuroprotective pathways that arise from the increase in Ang II formation are identified; the most acknowledged mechanism is via increase in angiotensin-II-type-2 (AT2) receptor stimulation.[5] The stimulation of AT2 receptors is believed to increase neuronal resistance to ischemia and promote collateral circulation recruitments after an ischemic event.[1,6] In addition, increase in Ang II formation leads to similar neuroprotective functions via upregulation of Angiotensin-(1–7) and stimulation of Mas receptors.[5]