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OtherCARDIOVASCULAR PHARMACOLOGY

Effects of Angiotensin II on Intracellular Calcium and Contracture in Metabolically Inhibited Cardiomyocytes

David R. Boston, Takashi Koyama, Jorge Rodriguez-Larrain, Anruo Zou, Zhi Su and William H. Barry
Journal of Pharmacology and Experimental Therapeutics May 1998, 285 (2) 716-723;
David R. Boston
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Takashi Koyama
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Jorge Rodriguez-Larrain
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Anruo Zou
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Zhi Su
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William H. Barry
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Abstract

Angiotensin II (A-II) is known to potentiate ischemic dysfunction during ischemia, but the mechanisms involved are not completely established. We examined the effects of A-II on intracellular calcium concentration ([Ca++]i) and cell contracture caused by metabolic inhibition in isolated adult rabbit ventricular myocytes. [Ca++]i was assessed by flow cytometry, using the Ca++-sensitive fluorescent probe, fluo-3. After 90 min of exposure to 2 mM cyanide (CN) and 0 glucose, there was a significant increase in myocyte [Ca++]i. This increase was slightly augmented in the presence of 100 nM A-II. In the presence of partial Na+/K+ ATP pump inhibition ([K+]o = 0.8 mM), there was a more significant increase in [Ca++]i associated with exposure to CN+A-II vs. CN alone. Similar results were obtained with CN plus 2-deoxyglucose, and the effect of A-II was inhibited by 10 μM 5-(N-ethyl-N-isopropyl)amiloride. Myocytes exposed to 2 mM CN and 0 glucose gradually developed contracture over a 3-hr period. Addition of 100 nM A-II significantly (P < .01) enhanced loss of rod shape morphology during 3 hr of CN exposure. Partial inhibition of the Na+ pump by exposure to 0.8 mM K+ had no effect on myocyte survival in the absence of CN, but augmented the harmful effect of A-II on cell contracture caused by CN exposure. This effect of A-II was completely reversed by the addition of 1 mM amiloride, a Na+/H+ exchange inhibitor. We conclude that A-II directly enhances cell injury during CN exposure in isolated rabbit ventricular myocytes. We postulate that this effect of A-II is mediated by stimulation of Na+/H+ exchange with resultant increased [Na+]i and subsequent [Ca++]i loading, possibly via reverse Na+/Ca++ exchange.

Footnotes

  • Send reprint requests to: Dr. William H. Barry, Cardiology Division, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, UT 84132.

  • ↵1 This work was supported by National Institutes of Health Grant HL-30478, and a Grant from Merck & Co., West Point, PA.

  • Abbreviations:
    A-II
    angiotensin II
    CN
    cyanide
    2DG
    2-deoxyglucose
    EIPA
    5-(N-ethyl-N-isopropyl) amiloride
    ACE
    angiotensin converting enzyme
    MKRBB
    modified Krebs-Ringer bicarbonate buffer
    MEM
    minimum essential medium
    HEPES
    [4-(2-hydroxyethyl)-1-piperazineethane-sulfonic acid
    DMSO
    dimethyl sulfoxide
    PI
    propidium iodide
    EGTA
    ethylene glycol-bis (β-aminoethyl ether)-N,N,N1,N1-tetraacetic acid
    • Received March 11, 1997.
    • Accepted January 14, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 285, Issue 2
1 May 1998
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OtherCARDIOVASCULAR PHARMACOLOGY

Effects of Angiotensin II on Intracellular Calcium and Contracture in Metabolically Inhibited Cardiomyocytes

David R. Boston, Takashi Koyama, Jorge Rodriguez-Larrain, Anruo Zou, Zhi Su and William H. Barry
Journal of Pharmacology and Experimental Therapeutics May 1, 1998, 285 (2) 716-723;

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OtherCARDIOVASCULAR PHARMACOLOGY

Effects of Angiotensin II on Intracellular Calcium and Contracture in Metabolically Inhibited Cardiomyocytes

David R. Boston, Takashi Koyama, Jorge Rodriguez-Larrain, Anruo Zou, Zhi Su and William H. Barry
Journal of Pharmacology and Experimental Therapeutics May 1, 1998, 285 (2) 716-723;
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