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The contribution of autonomic nervous system activity to the cardiovascular effects of delta-9-tetrahydrocannabinol (THC) was evaluated in 4 normal subjects. The peak heart rate rise after THC was attenuated by atropine and by propranolol, and nearly abolished by atropine-propranolol pretreatment. Blocking drugs also attenuated THC-induced changes in forearm blood flow and vascular resistance but did not affect changes in fingertip temperature. The data suggest that THC acts to induce sympathetic stimulation and parasympathetic inhibition of cardiovascular control pathways. Cardiovascular responses in an additional subject who developed hypertension after either intravenous or smoked marijuana are described.
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W Rogers, and
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N L Benowitz, and
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Clinical pharmacology and therapeutics,
N L Benowitz, and
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February 1981,
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N L Benowitz, and
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July 1987,
Life sciences,
N L Benowitz, and
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March 1977,
Clinical pharmacology and therapeutics,
N L Benowitz, and
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R T Jones
May 1975,
Clinical pharmacology and therapeutics,
N L Benowitz, and
J Rosenberg, and
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J Bachman, and
R T Jones
January 1984,
Biological research in pregnancy and perinatology,
N L Benowitz, and
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October 2007,
PLoS biology,
N L Benowitz, and
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The European journal of neuroscience,
N L Benowitz, and
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April 1992,
Brain research,
