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Research ArticleNEUROPHARMACOLOGY

Human Pharmacology of Ayahuasca: Subjective and Cardiovascular Effects, Monoamine Metabolite Excretion, and Pharmacokinetics

Jordi Riba, Marta Valle, Gloria Urbano, Mercedes Yritia, Adelaida Morte and Manel J. Barbanoj
Journal of Pharmacology and Experimental Therapeutics July 2003, 306 (1) 73-83; DOI: https://doi.org/10.1124/jpet.103.049882
Jordi Riba
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Marta Valle
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Gloria Urbano
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Mercedes Yritia
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Adelaida Morte
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Manel J. Barbanoj
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Abstract

The effects of the South American psychotropic beverage ayahuasca on subjective and cardiovascular variables and urine monoamine metabolite excretion were evaluated, together with the drug's pharmacokinetic profile, in a double-blind placebo-controlled clinical trial. This pharmacologically complex tea, commonly obtained from Banisteriopsis caapi and Psychotria viridis, combines N,N-dimethyltryptamine (DMT), an orally labile psychedelic agent showing 5-hydroxytryptamine2A agonist activity, with monoamine oxidase (MAO)-inhibiting β-carboline alkaloids (harmine, harmaline, and tetrahydroharmine). Eighteen volunteers with prior experience in the use of psychedelics received single oral doses of encapsulated freeze-dried ayahuasca (0.6 and 0.85 mg of DMT/kg of body weight) and placebo. Ayahuasca produced significant subjective effects, peaking between 1.5 and 2 h, involving perceptual modifications and increases in ratings of positive mood and activation. Diastolic blood pressure showed a significant increase at the high dose (9 mm Hg at 75 min), whereas systolic blood pressure and heart rate were moderately and nonsignificantly increased. Cmax values for DMT after the low and high ayahuasca doses were 12.14 ng/ml and 17.44 ng/ml, respectively. Tmax (median) was observed at 1.5 h after both doses. The Tmax for DMT coincided with the peak of subjective effects. Drug administration increased urinary normetanephrine excretion, but, contrary to the typical MAO-inhibitor effect profile, deaminated monoamine metabolite levels were not decreased. This and the negligible harmine plasma levels found suggest a predominantly peripheral (gastrointestinal and liver) site of action for harmine. MAO inhibition at this level would suffice to prevent first-pass metabolism of DMT and allow its access to systemic circulation and the central nervous system.

Footnotes

  • DOI: 10.1124/jpet.103.049882.

  • ABBREVIATIONS: DMT, N,N-dimethyltryptamine; THH, tetrahydroharmine; LSD, d-lysergic acid diethylamide; CNS, central nervous system; MAO, monoamine oxidase; COMT, catechol-O-methyltransferase; VMA, vanillylmandelic acid; HVA, homovanillic acid; 5-HIAA, 5-hydroxyindoleacetic acid; MDMA, methylenedioxymethamphetamine; HPLC, high-performance liquid chromatography; VAS, visual analog scale(s); HRS, Hallucinogen Rating Scale; ARCI, Addiction Research Center Inventory; MBG, morphine-benzedrine group; PCAG, pentobarbital-chlorpromazine-alcohol group; BG, benzedrine group; AUC, area under the concentration-time curve; CL/F, total plasma clearance; Vz/F, apparent volume of distribution; ANOVA, analysis of variance; SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate.

    • Received February 3, 2003.
    • Accepted March 13, 2003.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 306 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 306, Issue 1
1 Jul 2003
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Research ArticleNEUROPHARMACOLOGY

Human Pharmacology of Ayahuasca: Subjective and Cardiovascular Effects, Monoamine Metabolite Excretion, and Pharmacokinetics

Jordi Riba, Marta Valle, Gloria Urbano, Mercedes Yritia, Adelaida Morte and Manel J. Barbanoj
Journal of Pharmacology and Experimental Therapeutics July 1, 2003, 306 (1) 73-83; DOI: https://doi.org/10.1124/jpet.103.049882

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Research ArticleNEUROPHARMACOLOGY

Human Pharmacology of Ayahuasca: Subjective and Cardiovascular Effects, Monoamine Metabolite Excretion, and Pharmacokinetics

Jordi Riba, Marta Valle, Gloria Urbano, Mercedes Yritia, Adelaida Morte and Manel J. Barbanoj
Journal of Pharmacology and Experimental Therapeutics July 1, 2003, 306 (1) 73-83; DOI: https://doi.org/10.1124/jpet.103.049882
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