Cardiac Adrenoceptors : Physiological and Pathophysiological Relevance

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At present, nine adrenoceptor (AR) subtypes have been identified: α<sub>1A</sub>-, α<sub>1B</sub>-, α<sub>1D</sub>-, α<sub>2A</sub>-, α<sub>2B</sub>-, α<sub>2C</sub>-, β<sub>1</sub>-, β<sub>2</sub>-, and β<sub>3</sub>AR. In the human heart, β<sub>1</sub>- and β<sub>2</sub>AR are the most powerful physiologic mechanism to acutely increase cardiac performance. Changes in βAR play an important role in chronic heart failure (CHF). Thus, due to increased sympathetic activity in CHF, βAR are chronically (over)stimulated, and that results in β<sub>1</sub>AR desensitization and alterations of down-stream mechanisms. However, several questions remain open: What is the role of β<sub>2</sub>AR in CHF? What is the role of increases in cardiac G<sub>i</sub>-protein in CHF? Do increases in G-protein-coupled receptor kinase (GRK)s play a role in CHF? Does βAR-blocker treatment cause its beneficial effects in CHF, at least partly, by reducing GRK-activity? In this review these aspects of cardiac AR pharmacology in CHF are discussed. In addition, new insights into the functional importance of β<sub>1</sub>- and β<sub>2</sub>AR gene polymorphisms are discussed. At present it seems that for cardiovascular diseases, βAR polymorphisms do not play a role as disease-causing genes; however, they might be risk factors, might modify disease, and/or might influence progression of disease. Furthermore, βAR polymorphisms might influence drug responses. Thus, evidence has accumulated that a β<sub>1</sub>AR polymorphism (the Arg389Gly β<sub>1</sub>AR) may affect the response to βAR-blocker treatment.<br>

収録刊行物

  • Journal of pharmacological sciences  

    Journal of pharmacological sciences 100(5), 323-337, 2006-05-15 

    The Japanese Pharmacological Society

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各種コード

  • NII論文ID(NAID)
    10018237984
  • NII書誌ID(NCID)
    AA11806667
  • 本文言語コード
    ENG
  • 資料種別
    REV
  • ISSN
    13478613
  • NDL 記事登録ID
    7963144
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  CJP引用  NDL  J-STAGE 
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