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Fig. 1 | Experimental & Translational Stroke Medicine

Fig. 1

From: Therapeutic potential of the renin angiotensin system in ischaemic stroke

Fig. 1

Simplified overview of the renin angiotensin system (RAS). Angiotensinogen is cleaved by renin generating Angiotensin I (Ang I) which is then formed into Angiotensin II (Ang II) via the actions of angiotensin converting enzyme (ACE). Ang II preferentially binds to Angiotensin II type I receptor (AT1R) (‘classical axis’) inducing vasoconstriction, inflammation, oxidative stress, apoptosis and cell proliferation. Ang II can also activate the Angiotensin II type II (AT2R) and is metabolised by angiotensin converting enzyme 2 (ACE2) to generate Angiotensin-(1–7). Ang-(1–7) activates the Mas receptor (MasR). Ang-(1–7) can be formed by the actions of ACE or neprilysin (NEP) on Angiotensin-(1–9) or Angiotensin I. AT2R and ACE2/Ang-(1–7)/MasR form the ‘alternative axis’ and its activation is thought to counteract the detrimental effects induced by AT1R by leading to vasodilation, angiogenesis and preventing inflammation, oxidative stress and apoptosis

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