Abstract

The renin-angiotensin system (RAS) is a major physiological regulator of vascular tone and is implicated in cardiovascular pathophysiology. More recently, basic research has however continuously extended our understanding of the complexicity of the systemic and tissular RASs. The peptid hormone, angiotensin II, acts primarily via type I (AT1) and type II (AT2) angiotensin receptors. Most, if not all, of the peripheral and central actions of angiotensin II, including vasoconstriction, renal salt and water retention, facilitation of sympathetic transmission, modification of vascular and cardiac structure, oxydative stress stimulation and proinflammatory action were all thought to be mediated by the angiotensin type 1 receptor, AT1. Angiotensin II/III exerts actions through the AT2 receptor, which are directly opposed to those mediated by the AT1 receptor. Most notably, proteolytic fragments of angiotensin II also have biological activity via ther own receptors: angiotensin-(1-7)/AT1-7 and angiotensin IV/AT4. They are vasodilators in many arterial beds. The identification of these angiotensins opens the way to develop new therapeutics.

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