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Research ArticleCardiovascular

Acute Myocardial Infarction Inhibits the Neurogenic Tachycardic and Vasopressor Response in Rats via Presynaptic Cannabinoid Type 1 Receptor

Radosław Rudź, Eberhard Schlicker, Urszula Baranowska, Justyna Marciniak, Piotr Karabowicz and Barbara Malinowska
Journal of Pharmacology and Experimental Therapeutics October 2012, 343 (1) 198-205; DOI: https://doi.org/10.1124/jpet.112.196816
Radosław Rudź
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Eberhard Schlicker
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Urszula Baranowska
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Justyna Marciniak
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Piotr Karabowicz
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Barbara Malinowska
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland (R.R., U.B., J.M., P.K., B.M.); and Institute of Pharmacology and Toxicology, University of Bonn, Bonn, Germany (E.S.)
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Abstract

The present study was carried out to examine whether acute experimental myocardial infarction affects the sympathetic transmission to vessels and the heart of pithed rats via a presynaptic mechanism and, if so, to check whether inhibitory presynaptic cannabinoid (CB) receptors and endocannabinoids are involved in this response. In pithed and vagotomized rats, electrical stimulation (0.75 Hz; 1 ms; 50 V; 5 or 15 pulses for increases in heart rate or blood pressure, respectively) of the preganglionic sympathetic nerve fibers or intravenous injection of isoprenaline (0.1 nmol/kg) or noradrenaline (1 nmol/kg) increased heart rate and blood pressure by approximately 50 beats/min and 40 mm Hg, respectively. Ligation of the left coronary artery reduced the electrically (as opposed to the chemically) induced tachycardic and pressor responses by approximately 30 to 40%. The inhibitory effect of myocardial infarction was prevented by the CB1 receptor antagonist rimonabant but not by the CB2 receptor antagonist N-[(1S)-endo-1,3,3-trimethyl-bicyclo[2.2.1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyra-zole-3-carboxamide (SR144528) and the transient receptor potential vanilloid 1 receptor antagonist capsazepine. The inhibitory effect of myocardial infarction was slightly enhanced by the inhibitors of anandamide and 2-arachidonyl glycerol degradation, 3′-(aminocarbonyl)[1,1′-biphenyl]-3-yl)-cyclohexylcarbamate (URB597) and 4-nitrophenyl-4-(dibenzo[d][1,3]dioxol-5-yl(hydroxy)methyl)piperidine-1-carboxylate (JZL184), respectively. Rimonabant increased myocardial infarction-induced mortality. Our results demonstrate that during the early phase of myocardial infarction the activation of presynaptic CB1 receptors by endogenously formed cannabinoids contributes to the inhibition of the neurogenic tachycardic and vasopressor responses. Thus, the CB1 receptor-mediated inhibition of excessive noradrenaline release from the sympathetic nerve fibers innervating the heart and vessels might play a protective role in myocardial ischemia.

Footnotes

  • This work was supported by the Polish Ministry of Science and Higher Education [Grant 1339/POL/2006/30]; the Medical University of Białystok [Grant 3-13538F] (to B.M.); and the Copernicus Award from the Foundation for Polish Science (to B.M.) and the German Research Foundation (to E.S.).

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

    http://dx.doi.org/10.1124/jpet.112.196816.

  • ABBREVIATIONS:

    MI
    myocardial infarction
    AEA
    anandamide
    2-AG
    2-arachidonyl glycerol
    BP
    blood pressure
    DBP
    diastolic BP
    MBP
    mean BP
    SBP
    systolic BP
    CB
    cannabinoid
    DMSO
    dimethyl sulfoxide
    ES
    electrical stimulation
    FAAH
    fatty acid amide hydrolase
    HR
    heart rate
    ISO
    isoprenaline
    JZL184
    4-nitrophenyl-4-(dibenzo[d][1,3]dioxol-5-yl(hydroxy)methyl)piperidine-1-carboxylate
    MAGL
    monoacylglycerol lipase
    NA
    noradrenaline
    PGF2α
    prostaglandin F2α
    S
    stimuli
    SR144528
    N-[(1S)-endo-1,3,3-trimethyl-bicyclo[2.2.1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyra-zole-3-carboxamide
    TRPV
    transient receptor potential vanilloid
    URB597
    3′-(aminocarbonyl)[1,1′-biphenyl]-3-yl)-cyclohexylcarbamate
    VP
    vasopressin.

  • Received May 28, 2012.
  • Accepted July 12, 2012.
  • Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 343 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 343, Issue 1
1 Oct 2012
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Research ArticleCardiovascular

Myocardial Infarction and CB1 Receptors

Radosław Rudź, Eberhard Schlicker, Urszula Baranowska, Justyna Marciniak, Piotr Karabowicz and Barbara Malinowska
Journal of Pharmacology and Experimental Therapeutics October 1, 2012, 343 (1) 198-205; DOI: https://doi.org/10.1124/jpet.112.196816

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Research ArticleCardiovascular

Myocardial Infarction and CB1 Receptors

Radosław Rudź, Eberhard Schlicker, Urszula Baranowska, Justyna Marciniak, Piotr Karabowicz and Barbara Malinowska
Journal of Pharmacology and Experimental Therapeutics October 1, 2012, 343 (1) 198-205; DOI: https://doi.org/10.1124/jpet.112.196816
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