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血管紧张素Ⅱ在自发性高血压大鼠主动脉重建中的作用 被引量:5

Effect of angiotensin Ⅱ on the remodeling of aorta in spontaneously hypertensive rats
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摘要 目的 :探讨血管紧张素Ⅱ (AngⅡ )在高血压主动脉重建中的作用。方法 :选用AngⅡ受体I亚型拮抗剂losartan ,对雄性自发性高血压大鼠 (SHR)进行为期 10周的治疗 ,观察并比较其在剂量 15mg/kg·d-1及0 75mg/kg·d-1时 ,对 16周到 2 6周SHR胸主动脉重建的影响。结果 :Losartan 15mg在降低血压的同时 ,通过抑制主动脉中膜平滑肌细胞 (VSMC)的肥大明显抑制了主动脉肥厚 ,losartan 0 .75mg未能使血压下降的情况下 ,对VSMC及主动脉肥厚均没有影响。Losartan对胶原纤维的作用与对VSMC的作用不同 ,两种剂量的losartan均明显抑制了胶原纤维的合成。结论 :AngⅡ对SHR主动脉平滑肌生长的调节可能为压力依赖性 。 AIM: To investigate the effects of a 10-weeks treatment with angiotensin Ⅱ (Ang Ⅱ) subtype I receptor antagonist losartan on vascular remodeling of thoracic aorta in male spontaneously hypertensive rats (SHR). METHODS: SHR were treated from 16 to 26 weeks of age with losartan at 15 mg/kg·d -1 or 0.75 mg/kg·d -1. RESULTS: Losartan (15 mg/kg·d -1) treatment significantly decreased systolic blood pressure compared with the control group, while losartan (0.75 mg/kg·d -1) had no the effect, losartan(15 mg) prevents the development of aortic hypertrophy by preventing hypertrophy of vascular smooth muscle cells (VSMC). In the losartan 0.75 group, these parameters were not changed. But in the losartan 15 and losartan 0.75 groups, the collagen content of the aortic media decreased significantly. CONCLUSION: It is inferred that the effect of Ang Ⅱ on stimulating VSMC growth of the aorta in SHR is dependent on arterial pressure, while the effect on collagen fibers is through pressure independent mechanism.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2000年第3期214-217,共4页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助! (编号 :196 72 0 72 )
关键词 高血压 血管紧张素Ⅱ 大鼠 胶原纤维 Hypertension Blood vessels Angiotensin Ⅱ Muscle, smooth, vascular Cells Collagen
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  • 1卢对栋.现代分子生物学技术[M].北京:高等教育出版社,1995.135-238,408-429.
  • 2章建梁,杨向群.高血压血管重构[J].国外医学(心血管疾病分册),1997,24(1):26-29. 被引量:11
  • 3Lagami T, Murakami T, Higuchi K,et al. Role of vascular wall renin: intracellular and extracellular mechanism [J]. Blood Vessels, 1991, 28(1/2/3): 217 -223.
  • 4Numaguchi K, Egashira K, Takemuto M, et al. Chronic inhibition of nitric oxide synthesis causes coronary microvascular remodeling in rats [J]. Hy pertens,1995,26:957 - 962.
  • 5Van Bortel LM, Fici F, Mascagni F. Efficacy and tolerability of nebivolol compared with other antihypertensive drugs: a meta-analysis[J]. Am J Cardiovasc Drugs, 2008,8(1) :35-44.
  • 6Coekeroft J. A review of the safety and efficacy of nebivolol in the mildly hypertensive patient [J]. Vase Health Risk Manag ,2007,3(6):909-917.
  • 7Jin M, Wilhehn MJ, Lang RE, et al. Endogenous tissue renin-angiotensin systems, from molecular biology to therapy [J[. Am J Med,1988, 84 (3A): 28-36.
  • 8Morishita R, Gibbons GH, Ellison KE,et al. Evidence for direct local effect of angiotensin Ⅱ in vascular hypertrophy in vivo gene t ransfer of angiotensin converting enzyme [J]. J Clin Invest, 1995, 94 (3): 978-984.
  • 9Veverka A, Salinas JL. Nebivolol in the treatment of chronic heart failure[J]. Vasc Health Risk Manag,2007,3(5) :647-654.
  • 10Altwegg I.A, d'Uscio LV, Barandier C, et al. Nebivolol induces NO-mediated relaxations of rat small mesenteric but not of large elastic arteries [J]. J Cardiovasc Pharmacol,2000, 36(3):316-320.

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