The renin–angiotensin system (RAS) plays a central role in the regulation of blood pressure and electrolyte homoeostasis.1 At the first and rate-limiting step of the RAS cascade, renin, a highly specific aspartyl protease, cleaves angiotensinogen, produced in the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE (Angiotensin Converting Enzyme). Angiotensin II constricts blood vessels leading to increased blood pressure. It also increases the secretion of ADH and aldosterone, and stimulates the hypothalamus to activate the thirst reflex. Since an overactive renin-angiotensin system leads to hypertension, renin is an attractive target for the treatment of this disease. 2-4
References:
1. He, FJ. and GA. MacGregor, J. Renin Angiotensin Aldosterone Syst. 4, 11 (2003).
2. Wood, JM. et al., Hypertension, 7, 797 (1985).
3. Shibasaki, M. et al., Am. J. Hypertens. 4, 932 (1991).
4. Wood, JM.et al., Biochem. Biophys. Res. Comm. 308, 698 (2003).
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