High blood pressure, or hypertension, afflicts an estimated one in four American adults. This condition puts a strain on the heart and blood vessels and greatly increases the risk of stroke and heart disease.

Emerging research indicates that the endogenous cannabinoid system plays a role in regulating blood pressure, though its mechanism of action is not well understood.[1] Animal studies demonstrate that anandamide and other endocannabinoids profoundly suppress cardiac contractility in hypertension and can normalize blood pressure,[2-3] leading some experts to speculate that the manipulation of the endocannabinoid system "may offer novel therapeutic approaches in a variety of cardiovascular disorders."[4]


The administration of natural cannabinoids has yielded conflicting cardiovascular effects on humans and laboratory animals.[5-9] The vascular response in humans administered cannabis in experimental conditions is typically characterized by a mild increase in heart rate and blood pressure. However, complete tolerance to these effects develops quickly and potential health risks appear minimal.[10-11]

In animals, cannabinoid administration in animals is typically associated with vasodilation, transient bradycardia and hypotension,[12] as well as an inhibition of atherosclerosis (hardening of the arteries) progression.[13-15] The administration of synthetic cannabinoids have also been shown to lower blood pressure in animals and have not been associated with cardiotoxicity in humans.[16]

At this time, research assessing the clinical use of cannabinoids for hypertension is in its infancy though further investigation appears warranted.[17]



[1] Franjo Grotenhermen. 2006. Clinical pharmacodynamics of cannabinoids. In Russo et al (Eds) Handbook of Cannabis Therapeutics. Binghampton, New York: Haworth Press.

[2] Batkai et al. 2004. Endocannabinoids acting at cannabinoid-1 receptors regulate cardiovascular function in hypertension. Circulation 110: 1996-220.

[3] Pacher et al. 2005. Blood pressure regulation by endocannabinoids and their receptors (PDF). Neuropharmacology 48: 1130-1138.

[4] Ibid.

[5] Cecilia Hillard. 2000. Endocannabinoids and vascular function. Journal of Pharmacology and Experimental Therapeutics. 294: 27-32.

[6] Kunos et al. 2000. Endocannabinoids as cardiovascular modulators. Chemistry and Physics of Lipids 108: 159-168.

[7] Reese Jones. 2002. Cardiovascular system effects of marijuana. Journal of Clinical Pharmacology. 42: 58-63.

[8] Ribuot et al. 2005. Cardiac and vascular effects of cannabinoids: toward a therapeutic use? Annales de Cardiologie et d’Angeiologie (France) 54: 89-96.

[9] Steven Karch. 2006. Cannabis and cardiotoxicity. Forensic Science, Medicine, and Pathology. 2: 13-18.

[10] Ibid.

[11] Rodondi et al. 2006. Marijuana use, diet, body mass index and cardiovascular risk factors. American Journal of Cardiology 98: 478-484.

[12] Reese Jones. 2002. op. cit.

[13] Steffens and Mach. 2006. Towards a therapeutic use of selective CB2 cannabinoid receptor ligands for atherosclerosis. Future Cardiology 2: 49-53.

[14] Steffens et al. 2005. Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. Nature 434: 782-786.

[15] Steffens and Mach. 2006. Cannabinoid receptors in atherosclerosis. Current Opinion in Lipidology 17: 519-526.

[16] Steven Karch. 2006. op. cit.

[17]Francois Mach. 2006. New anti-inflammatory agents to reduce atherosclerosis. Archives of Physiology and Biochemistry 112: 130-137.

Reprinted with Permission of National NORML