A series of 2-alkylbenzimidazole derivatives 9a-n have been designed and synthesized as a novel class of non-peptide angiotensin H AT1 receptor antagonists. The synthesized compounds were evaluated for their antagonis...A series of 2-alkylbenzimidazole derivatives 9a-n have been designed and synthesized as a novel class of non-peptide angiotensin H AT1 receptor antagonists. The synthesized compounds were evaluated for their antagonism of angiotensin H, induced contraction in the rabbit thoracic aortic ring and the results showed that compounds 9a, 9g and 9j exhibited potent antagonistic activity of AT1 receptor.展开更多
目的探讨应激性心肌病发生时血清血管紧张素Ⅱ水平的变化,并观察血管紧张素Ⅱ受体拮抗药缬沙坦在防治应激性心肌病的作用。方法 18只2周龄的雌性大白兔随机分为对照组、实验组和干预组,在0、7和14 d抽血,酶联免疫法吸附试验(enzymelinke...目的探讨应激性心肌病发生时血清血管紧张素Ⅱ水平的变化,并观察血管紧张素Ⅱ受体拮抗药缬沙坦在防治应激性心肌病的作用。方法 18只2周龄的雌性大白兔随机分为对照组、实验组和干预组,在0、7和14 d抽血,酶联免疫法吸附试验(enzymelinked immunosorbent assay,ELISA)检测血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)浓度变化;第14天Western blot检测血管紧张素Ⅱ一型受体(angiotensinⅡreceptor t y pe 1,AT1)、血管紧张素Ⅱ二型受体(angiotensinⅡreceptor type 2,AT2)的表达;HE染色观察各组心肌组织变化情况。结果在0、7和14 d,实验组和干预组的血清中A ngⅡ浓度显著高于对照组(P<0.05);第14天实验组心尖组织AT1表达较对照组显著降低(P<0.05),而干预组与对照组相比差异无统计学意义。实验组和干预组AT2表达较对照组显著升高(P<0.05)。HE染色显示实验组动物心尖部游离壁较对照组显著变薄(P<0.05),而干预组与对照组差异无统计学意义;实验组心尖部心肌组织可见典型的应激性心肌病心肌改变,干预组无此变化。结论 AngⅡ可能参与了应激性心肌病的发生,AT1受体拮抗药缬沙坦可以防治应激性心肌病的发生。展开更多
基金We are thankful to the National Natural Science Foundation of China(No.30371688)Key Fund of Ministry of Education of China(No.03089)for financial support.
文摘A series of 2-alkylbenzimidazole derivatives 9a-n have been designed and synthesized as a novel class of non-peptide angiotensin H AT1 receptor antagonists. The synthesized compounds were evaluated for their antagonism of angiotensin H, induced contraction in the rabbit thoracic aortic ring and the results showed that compounds 9a, 9g and 9j exhibited potent antagonistic activity of AT1 receptor.
文摘目的探讨应激性心肌病发生时血清血管紧张素Ⅱ水平的变化,并观察血管紧张素Ⅱ受体拮抗药缬沙坦在防治应激性心肌病的作用。方法 18只2周龄的雌性大白兔随机分为对照组、实验组和干预组,在0、7和14 d抽血,酶联免疫法吸附试验(enzymelinked immunosorbent assay,ELISA)检测血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)浓度变化;第14天Western blot检测血管紧张素Ⅱ一型受体(angiotensinⅡreceptor t y pe 1,AT1)、血管紧张素Ⅱ二型受体(angiotensinⅡreceptor type 2,AT2)的表达;HE染色观察各组心肌组织变化情况。结果在0、7和14 d,实验组和干预组的血清中A ngⅡ浓度显著高于对照组(P<0.05);第14天实验组心尖组织AT1表达较对照组显著降低(P<0.05),而干预组与对照组相比差异无统计学意义。实验组和干预组AT2表达较对照组显著升高(P<0.05)。HE染色显示实验组动物心尖部游离壁较对照组显著变薄(P<0.05),而干预组与对照组差异无统计学意义;实验组心尖部心肌组织可见典型的应激性心肌病心肌改变,干预组无此变化。结论 AngⅡ可能参与了应激性心肌病的发生,AT1受体拮抗药缬沙坦可以防治应激性心肌病的发生。
文摘为研究罗沙坦对高血压冠状动脉壁肥厚的逆转作用，将16 周大鼠分为自发性高血压大鼠(SHR)组、SHR 口服大剂量罗沙坦组[ 15mg/kg/d)]、SHR 口服小剂量罗沙坦组[0.75mg/kg.d)] 和正常血压大鼠(WKY)组，饲养10 周。结果显示大剂量罗沙坦治疗显著降低SHR 的收缩压，降低冠状动脉壁横截面积、横截面积与内径比，提高最大冠状动脉流量，小剂量罗沙坦治疗对SHR 的收缩压，外径>200 m m 冠状动脉壁横截面积、横截面积与内径比，及最大冠状动脉流量低下无影响，但能显著降低外径<200 m m 冠状动脉壁横截面积、横截面积与内径比。
