4474-91-3
基本信息
血管緊張素2
血管緊張肽酰胺
血管緊張肽II
血管緊張素II
人血管緊張素II
血管緊張素Ⅱ雜質(zhì)
醋酸血管緊張素II
血管緊張素II(人)
增血壓素,HYPERTENSIN
DRVYIHPF
TY-10721
ANGIOTENSIN-2
H-DRVYIHPF-OH
ANGIOTENSIN II
angiotensin renin
ANTI-ANGIOTENSIN II
ile(5)-angiotensini
[ILE5]-ANGIOTENSIN 2
物理化學(xué)性質(zhì)
應(yīng)用領(lǐng)域
不良反應(yīng)和禁忌:有時(shí)可引起眩暈、頭痛,偶致心絞痛。過(guò)量可致心動(dòng)過(guò)緩。失血過(guò)多引起的低血壓應(yīng)補(bǔ)充血容量。心功能不全者慎用。
制備方法
取芐氧羰酰苯丙氨酸叔丁酯溶于甲醇,加入5%鈀炭,不斷振搖下通入氫氣6h,然后過(guò)濾,濾液濃縮至干,得苯丙氨酸叔丁酯。
另取等摩爾芐氧羰酰脯氨酸和苯丙氨酸叔丁酯溶于乙酸乙酯中,冰浴冷卻,加入適量二環(huán)己基碳二亞胺,冷藏2天,取出過(guò)濾去雜質(zhì),濾液以枸櫞酸、氯化鈉、碳酸氫鈉、氯化鈉溶液分別依次洗滌3次,用無(wú)水硫酸鈉干燥,濃縮,得芐氧羰酰脯·苯丙叔丁酯。
將芐氧羰酰脯·苯丙叔丁酯溶于甲醇,加入鈀炭(5%),通人氫氣振搖6h,然后過(guò)濾,濾液濃縮至干,得脯·苯丙叔丁酯。
取芐氧羰酰纈氨酰組氨酸酰肼溶于2mol/L鹽酸中,加入乙酸乙酯,在0℃下加入過(guò)量的亞硝酸鈉溶液(10%)反應(yīng)10min,用碳酸鉀調(diào)節(jié)pH 9以上,加入乙酸乙酯提取3次,合并提取液,用氯化鈉溶液洗滌提取液,無(wú)水硫酸鈉干燥,得芐氧羰酰纈·組疊氮。
把芐氧羰酰纈·組疊氮液體倒人脯·苯丙叔丁酯中,置冰箱2天,然后用枸櫞酸、氯化鈉、碳酸氫鈉、氯化鈉液依次分別洗滌,用無(wú)水硫酸鈉干燥,得芐氧羰酰纈·組·脯·苯丙叔丁酯,然后將其溶于甲醇中,加入5%鈀炭,通人氫氣,并不斷振搖6h,反應(yīng)完畢后,過(guò)濾,濾液濃縮,得纈·組·脯·苯丙叔丁酯。
取芐氧羰酰纈氨酰酪氨酸酰肼溶于二甲基甲酰胺-乙酸乙酯—鹽酸混合液中,于-20℃下慢慢加入亞硝酸叔丁醇,攪拌10min后用三乙胺調(diào)節(jié)至中性,過(guò)濾,得芐氧羰酰纈·酪疊氮濾液。
濾液加入纈·組·脯·苯丙叔丁酯中,冷藏2天,加人大量乙醚。過(guò)濾沉淀,干燥即得芐氧羰酰纈·酪·纈·組·脯·苯丙叔丁酯。
將芐氧羰酰纈·酪·纈·組·脯·苯丙叔丁酯溶于甲醇中,加入10%鈀炭,通入氫氣,并不斷振搖6h后,過(guò)濾,濾液濃縮,得芐氧羰酰纈·酪·纈·組·脯·苯丙叔丁酯。
取芐氧羰酰天冬酰胺酰硝基精氨酸和芐氧羰酰纈·酪·纈·組·脯·苯丙叔丁酯溶于二甲基甲酰胺中,加入二環(huán)己基碳二亞胺溶液,于35℃保溫3天。過(guò)濾,濾液加入碳酸氫鈉溶液,得白色沉淀,過(guò)濾,沉淀物用乙醇-乙醚混合液洗滌,得酪·纈·組·脯·苯丙叔丁酯。
將酪·纈·組·脯·苯丙叔丁酯加入三氟乙酸中,于30℃振搖4h,然后加入無(wú)水乙醚,收集沉淀干燥,得芐氧羰酰天胺·硝基精·纈·酪·纈·組·脯·苯丙。
將芐氧羰酰天胺·硝基精·纈·酪·纈·組·脯·苯丙溶于甲醇-鹽酸中,加入鈀炭,通人氫氣振搖8h,反應(yīng)完畢,過(guò)濾,濾液用弱堿性苯乙烯系陰離子交換樹(shù)脂303×2(704)調(diào)節(jié)pH至中性,過(guò)濾,濾液濃縮至干,乙醚洗滌,過(guò)濾,干燥,即得增血壓素,生物活力達(dá)60%以上。
上下游產(chǎn)品信息
常見(jiàn)問(wèn)題列表
Angiotensin receptor (AT receptor)
Most of the known actions of Angiotensin II (Ang II) are mediated by AT 1 receptors, the AT 2 receptor contributes to the regulation of blood pressure and renal function. 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 (AT 1 ). At the cellular level, responsiveness to Angiotensin II is conferred by the expression of the two classes of angiotensin receptors (AT 1 and AT 2 ). The effects of Angiotensin II to increase blood pressure are mediated by AT1 receptors.
To distinguish the AT 1 receptor 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 AT 1 receptors in the kidney promoting sodium reabsorption.