Upregulation of Angiotensin-Converting Enzyme 2 After Myocardial Infarction by Blockade of Angiotensin II Receptors

DOI Web Site 被引用文献21件
  • Yuichiro Ishiyama
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.
  • Patricia E. Gallagher
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.
  • David B. Averill
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.
  • E. Ann Tallant
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.
  • K. Bridget Brosnihan
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.
  • Carlos M. Ferrario
    From the Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC.

抄録

<jats:p> We investigated in Lewis normotensive rats the effect of coronary artery ligation on the expression of cardiac angiotensin-converting enzymes (ACE and ACE 2) and angiotensin II type-1 receptors (AT <jats:sub>1a</jats:sub> -R) 28 days after myocardial infarction. Losartan, olmesartan, or the vehicle (isotonic saline) was administered via osmotic minipumps for 28 days after coronary artery ligation or sham operation. Coronary artery ligation caused left ventricular dysfunction and cardiac hypertrophy. These changes were associated with increased plasma concentrations of angiotensin I, angiotensin II, angiotensin-(1–7), and serum aldosterone, and reduced AT <jats:sub>1a</jats:sub> -R mRNA. Cardiac ACE and ACE 2 mRNAs did not change. Both angiotensin II antagonists attenuated cardiac hypertrophy; olmesartan improved ventricular contractility. Blockade of the AT <jats:sub>1a</jats:sub> -R was accompanied by a further increase in plasma concentrations of the angiotensins and reduced serum aldosterone levels. Both losartan and olmesartan completely reversed the reduction in cardiac AT <jats:sub>1a</jats:sub> -R mRNA observed after coronary artery ligation while augmenting ACE 2 mRNA by approximately 3-fold. Coadministration of PD123319 did not abate the increase in ACE 2 mRNA induced by losartan. ACE 2 mRNA correlated significantly with angiotensin II, angiotensin-(1–7), and angiotensin I levels. These results provide evidence for an effect of angiotensin II blockade on cardiac ACE 2 mRNA that may be due to direct blockade of AT <jats:sub>1a</jats:sub> receptors or a modulatory effect of increased angiotensin-(1–7). </jats:p>

収録刊行物

  • Hypertension

    Hypertension 43 (5), 970-976, 2004-05

    Ovid Technologies (Wolters Kluwer Health)

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