"目录号: HY-13948
Angiotensin II human 是由Angiotensin I经过血管紧张素转换酶(ACE)催化移除C末端残基而得到。Angiotensin II 由AT1和AT2受体调节。
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生物活性
Description
Angiotensin II human is converted by Angiotensin I through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE). Angiotensin II is mediated byAT1andAT2receptors, which are seven transmembrane glycoproteins with 30% sequence similarity.
IC50& Target
Angiotensin receptor (AT receptor)[1]
In Vitro
Most of the known actions of Angiotensin II (Ang II) are mediated by AT1receptors, the AT2receptor contributes to the regulation of blood pressure and renal function[1]. Angiotensin II raises blood pressure (BP) by a number of actions, the most important ones being vasoconstriction, sympathetic nervous stimulation, increased aldosterone biosynthesis and renal actions. Other Angiotensin II actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. These actions are mediated by type 1 Ang II receptors (AT1)[2]. At the cellular level, responsiveness to Angiotensin II is conferred by the expression of the two classes of angiotensin receptors (AT1and AT2). The effects of Angiotensin II to increase blood pressure are mediated by AT1 receptors[3].
In Vivo
To distinguish the AT1receptor population that is critical for the pathogenesis of hypertension, osmotic minipumps are implanted s.c. into each animal to infuse Angiotensin II (1,000 ng/kg/min) continuously for 4 weeks. Angiotensin II causes hypertension by activating AT1receptors in the kidney promoting sodium reabsorption[3].
References