Figure 2.

The renin-angiotensin-system and ACE2. Triggered by low blood pressure, low blood volume and low sodium levels as well as sympathetic activity, the kidney secretes renin. Renin, a protease, cleaves angiotensinogen, secreted by the liver, into angiotensin I. Angiotensin I is then converted by the angiotensin-converting enzyme, which can be found in membranes of endothelial cells most abundantly in the lungs and kidneys, into angiotensin II. Various effects are caused by angiotensin II, which ultimately result in an increase of blood pressure and volume. The angiotensin-converting enzyme 2 works as a counterbalance to ACE by cleaving angiotensin I and angiotensin II into Ang 1–9* and Ang 1–7, respectively. (*Ang1–9 is postulated to exert similar effects as Ang1–7, though current data is limited and needs further validation). Activation of this pathway leads to vasodilation, inhibits cell proliferation and has anti-inflammatory effects. During pregnancy, maternal and fetal tissues contribute to the production of ACE2, leading to systemic vasodilation.