Hypertension, or high blood pressure, afflicts an estimated one in four American adults. The condition puts a strain on the human heart and blood vessels and considerably increases the risk of stroke and heart disease.
The endogenous cannabinoid system plays a role in regulating blood pressure as per emerging research, though its mechanism of action is not well understood. It is being demonstrated by animal studies that anandamide and other endocannabinoids profoundly suppress cardiac contractility in hypertension and may normalize blood pressure, which encourages some experts to speculate that the manipulation of the endocannabinoid system "may offer novel therapeutic approaches in a variety of cardiovascular disorders."
On humans and laboratory animals, the administration of natural cannabinoids has yielded conflicting cardiovascular effects. The vascular response in humans administered cannabis in experimental conditions is generally characterized by a mild increase in heart rate and blood pressure. However, complete tolerance to these effects develops quickly and potential health risks appear to be minimal. In animals, the administration of cannabinoids is usually associated with vasodilation, transient bradycardia and hypotension, besides an inhibition of atherosclerosis (hardening of the arteries) progression. Synthetic cannabinoid administration has also been shown for lowering blood pressure in animals and has not been associated with cardiotoxicity in humans.
References:
[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.
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