Abstract
The activity of the renin-angiotensin-aldosterone (RAA) system is thought to play a significant role in the development of cardiovascular atherosclerotic and hypertensive disease. The RAA system plays an important role in the regulation of blood pressure, cardiac and arterial structure [1] and salt and water homeostasis. Also, this system is well-known to be involved in the control of blood pressure and the pathogenesis of several forms of experimental and human hypertension. Angiotensinogen is cleaved by renin to produce the inactive peptide angiotensin I [2]. The ACE then converts angiotensin I (Ang I) to angiotensin II (Ang II), the latter peptide has various effects including vasoconstriction, aldosterone production, and enhanced noradrenalin release from sympathetic nerve endings. Ang II has also hypertrophic, and possibly hyperplastic, effects on vascular smooth muscle cells and cardiomyocytes [3], and increases extracellular collagen matrix synthesis.
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Lajemi, M., Benetos, A. (2001). Genetics of the renin-angiotensin-aldosterone system and risk of arterial disease. In: D’Orléans-Juste, P., Plante, G.E. (eds) ACE Inhibitors. Milestones in Drug Therapy MDT. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-7579-0_2
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