Background:
Angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe | His-Leu) is an octapeptide that is converted from Angiotensin I (AI) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial and kidney epithelial cells).
Angiotensin II has been shown to play important roles in mediating hypertension, heart failure, cardiac remodeling, diabetes, and the proliferative and inflammatory responses to arterial injury [1].
Angiotensin II exerts a wide range of effects on the cardiovascular system. It is a potent vasopressor and a powerful stimulus for production and release of aldosterone from the adrenal cortex. It acts via specific receptors in the adrenal glands to stimulate the secretion of aldosterone, which stimulates salt and water reabsorption by the kidneys. Angiotensin increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates contraction by an IP3-dependent mechanism). It was demonstrated that Ang II activated phospholipase C, resulting in the production of inositol trisphosphate (IP3) and diacylglycerol, which in turn were responsible for the mobilization of [Ca2+]i and the activation of PKC, respectively. Additional studies in SMC cultures examined the properties of Ang II as a growth agonist, in particular its role in promoting cellular hypertrophy, characterized by increases in protein synthesis, cell size, and polyploidy. [2][3]
参考文献:
1. Ruiz-Ortega M, Lorenzo O, Ruperez M, Esteban V, Suzuki Y, Mezzano S, Plaza JJ, Egido J. Role of the renin-angiotensin system in vascular diseases: expanding the field. Hypertension. 2001; 38: 1382-1387.
2. Geisterfer AA, Peach MJ, Owens GK. Angiotensin II induces hypertrophy, not hyperplasia, of cultured rat aortic smooth muscle cells. Circ Res. 1988; 62: 749-756.
3. Berk BC, Vekshtein V, Gordon HM, Tsuda T. Angiotensin II-stimulated protein synthesis in cultured vascular smooth muscle cells. Hypertension. 1989; 13: 305-314.
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