The renin angiotensin system (RAS), a homeostatic system involved in blood pressure and volume control, is implicated in the pathology of several risk factors for ischaemic stroke. Mounting evidence now suggests that the RAS may play a role in the pathophysiology of ischaemic stroke. This is thought to be due to an imbalance between the classical RAS axis, Angiotensin converting enzyme/Angiotensin II/Angiotensin II receptor type I (ACE/Ang II/AT1R), and the counter-regulatory RAS axis, Angiotensin converting enzyme 2/Angiotensin-(1-7)/Mas receptor [ACE2/Ang-(1-7)/MasR]. The counter- regulatory axis has been shown to provide neuroprotection in ischaemic stroke animal models. Therefore, the studies conducted in this thesis aimed to test the neuroprotective potential of Ang-(1-7) as a post-stroke therapy following transient focal cerebral ischaemia. Furthermore, experiments were conducted to test a potential synergistic effect between MasR and alternative Ang II receptor, Angiotensin II receptor type II (AT2R), agonism following stroke.
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Cerebral damage following ischaemic stroke: the role of Angiotensin-(1-7)