[On angiotensin II receptor distribution after myocardial infarction in dogs].

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  • Author(s): Qu XF;Qu XF; Li JJ; Xi Y; Shen JX; Xiu CH; Yue L; Wang GZ; Huang YL
  • Source:
    Zhonghua xin xue guan bing za zhi [Zhonghua Xin Xue Guan Bing Za Zhi] 2009 Apr; Vol. 37 (4), pp. 358-62.
  • Publication Type:
    English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    Chinese
  • Additional Information
    • Source:
      Publisher: Zhonghua yi xue hui Country of Publication: China NLM ID: 7910682 Publication Model: Print Cited Medium: Print ISSN: 0253-3758 (Print) Linking ISSN: 02533758 NLM ISO Abbreviation: Zhonghua Xin Xue Guan Bing Za Zhi Subsets: MEDLINE
    • Publication Information:
      Original Publication: Beijing, Zhonghua yi xue hui [1973?]-
    • Subject Terms:
    • Abstract:
      Objective: To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI).
      Methods: Canines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan.
      Conclusion: Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.
    • Accession Number:
      0 (Angiotensin II Type 1 Receptor Blockers)
      0 (RNA, Messenger)
      0 (Receptor, Angiotensin, Type 1)
      0 (Receptor, Angiotensin, Type 2)
      0 (Tetrazoles)
      80M03YXJ7I (Valsartan)
      HG18B9YRS7 (Valine)
    • Publication Date:
      Date Created: 20091002 Date Completed: 20100107 Latest Revision: 20151119
    • Publication Date:
      20240829
    • Accession Number:
      19791474