Cardiovascular effects of intravenous delta-9-tetrahydrocannabinol: autonomic nervous mechanisms.
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.
D000328:Adult; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D013759:Dronabinol / Q000494:pharmacology*; D004347:Drug Interactions; D000431:Ethanol / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D012881:Skin Temperature / Q000187:drug effects; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D000431:Ethanol; D001285:Atropine; D013759:Dronabinol; D011433:Propranolol