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The goal of the present review is to examine the evidence for beneficial actions of manipulation of the RAS (renin–angiotensin system) in stroke, with particular focus on Ang-(1–7) [angiotensin-(1–7)] and its receptor Mas. The RAS appears to be highly involved in the multifactorial pathophysiology of stroke. Blocking the effects of AngII (angiotensin II) at AT₁R (AngII type 1 receptor), through the use of commonly prescribed ACE (angiotensin-converting enzyme) inhibitors or AT₁R blockers, has been shown to have therapeutic effects in both ischaemic and haemorrhagic stroke. In contrast with the deleterious actions of over activation of AT₁R by AngII, stimulation of AT₂Rs (AngII type 2 receptors) in the brain has been demonstrated to elicit beneficial effects in stroke. Likewise, the ACE2/Ang-(1–7)/Mas axis of the RAS has been shown to have therapeutic effects in stroke when activated, countering the effects of the ACE …