Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Modulates Coronary Release of Tissue Plasminogen Activator in Response to Bradykinin

DOI PubMed 被引用文献5件 参考文献48件
  • OHIRA Naoto
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • MATSUMOTO Tetsuya
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • TAMAKI Shinji
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • TAKASHIMA Hiroyuki
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • TARUTANI Yasuhiro
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • YAMANE Tetsunobu
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • YASUDA Yo
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science
  • HORIE Minoru
    Department of Cardiovascular-Respiratory Medicine, Shiga University of Medical Science

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The aim of this study was to assess the relationship between the angiotensin converting enzyme gene (ACE) genotype and endothelium-dependent coronary vasomotor and fibrinolytic activity. The ACE DD genotype has been reported to be a risk factor for myocardial infarction. However, the mechanism is unknown. The fibrinolytic and renin-angiotensin systems are linked via ACE at the vascular beds. We studied 73 patients (II: n =24; ID: n =37; DD: n =12) who underwent diagnostic cardiac catheterization. Graded doses of bradykinin (BK) (0.2, 0.6, 2.0μg/min) and acetylcholine (30,100μg/min) were administered into the left coronary artery. Coronary blood flow (CBF) was evaluated by measuring Doppler flow velocity. Blood samples were taken from the aorta (Ao) and the coronary sinus (CS). Coronary release of tPA antigen was determined as a CS-Ao gradient×CBF×[(100-hematocrit) / 100]. ACE genotypes were determined using polymerase chain reaction. The ACE genotype did not appear to affect coronary macro- and microvascular responses induced by BK or acetylcholine. Coronary tissue plasminogen activator (tPA) release induced by BK was depressed in subjects with the ACE DD genotype. ACE levels in the DD genotype were significantly higher than those in the ID or II genotype. In all of the subjects, there was a significant negative correlation between the serum level of ACE activity and net coronary tPA release in response to BK at 0.6μg/min. In conclusions, the DD genotype of the ACE gene impairs the coronary release of tPA induced by BK. (Hypertens Res 2004; 27: 39-45)

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