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Related Experiment Video

Updated: Jan 3, 2026

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Alcohol Binge-Induced Cardiovascular Dysfunction Involves Endocannabinoid-CB1-R Signaling.

Janos Paloczi1, Csaba Matyas1, Resat Cinar2

  • 1Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, Maryland.

JACC. Basic to Translational Science
|November 27, 2019
PubMed
Summary

Excessive alcohol binge drinking causes significant cardiovascular dysfunction in mice. This effect involves endocannabinoid-cannabinoid 1 receptor (CB1-R) signaling, highlighting a potential therapeutic target.

Keywords:
2-AG, 2-arachidonyl glycerolAEA, anandamideCB1-R (CB1), cannabinoid 1 receptorCB2-R (CB2), cannabinoid 2 receptorEF, ejection fractionLV, left ventricleMAP, mean arterial pressureP-V, pressure-volumePRSW, preload recruitable stroke workTPR, total peripheral resistancebinge alcohol drinkingcannabinoidscontractilitydP/dtmax, maximal slope of pressure incrementendocannabinoids

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Area of Science:

  • Cardiovascular Physiology
  • Neuroendocrinology
  • Pharmacology

Background:

  • Excessive alcohol consumption, particularly binge drinking, poses significant risks to cardiovascular health.
  • The endocannabinoid system, including cannabinoid 1 receptor (CB1-R) signaling, plays a role in various physiological processes, but its specific impact on alcohol-induced cardiovascular dysfunction is not fully understood.

Purpose of the Study:

  • To comprehensively characterize the hemodynamic consequences of an acute alcohol binge in a mouse model.
  • To elucidate the involvement of endocannabinoid-cannabinoid 1 receptor (CB1-R) signaling in mediating these cardiovascular effects.

Main Methods:

  • Acute alcohol binge administration in mice.
  • Multimodal hemodynamic monitoring to assess cardiovascular function.
  • Measurement of cardiac endocannabinoid levels, specifically anandamide.
  • Pharmacological blockade of CB1-R using an antagonist.
  • Assessment of cardiovascular parameters in CB1-R knockout mice.

Main Results:

  • An acute alcohol binge induced profound and prolonged cardiovascular dysfunction, including circulatory redistribution, lasting several hours.
  • Cardiac levels of the endocannabinoid anandamide were elevated following the alcohol binge.
  • Administration of a CB1-R antagonist significantly attenuated the alcohol-induced cardiovascular dysfunction.
  • Cardiovascular dysfunction was markedly reduced in CB1-R knockout mice compared to wild-type controls.

Conclusions:

  • A single episode of binge alcohol drinking exerts substantial adverse effects on the cardiovascular system.
  • Endocannabinoid-CB1-R signaling is a critical mediator of alcohol binge-induced cardiovascular dysfunction.
  • Targeting the endocannabinoid-CB1-R pathway may offer a novel therapeutic strategy for mitigating the cardiovascular consequences of alcohol abuse.