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Am J Physiol Heart Circ Physiol (April 8, 2005). doi:10.1152/ajpheart.00107.2005
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Submitted on February 2, 2005
Accepted on April 4, 2005

Hemodynamic profile, responsiveness to anandamide and baroreflex sensitivity of mice lacking fatty acide amide hydrolase

Pal Pacher1*, Sandor Batkai1, Douglas Osei-Hyiaman1, Laszlo Offertaler1, Jie Liu1, Judy Harvey-White1, Attila Brassai1, Zoltan Jarai1, Benjamin F Cravatt2, and George Kunos1

1 Laboratory of Physiologic Studies, NIH/NIAAA, USA
2 Department of Cell Biology, The Scripps Research Institut, USA

* To whom correspondence should be addressed. E-mail: pacher{at}mail.nih.gov.

The endocannabinoid anandamide exerts neurobehavioral, cardiovascular and immune-regulatory effects through cannabinoid receptors (CB). Fatty acid amide hydrolase (FAAH) is an enzyme responsible for the in vivo degradation of anandamide. Recent experimental studies have suggested that targeting the endocannabinergic system by FAAH inhibitors is a promising novel approach for the treatment of anxiety, inflammation and hypertension. In this study we compared the cardiac performance of FAAH knockout (FAAH-/-) mice and their wild-type (FAAH+/+) littermates, and analyzed the hemodynamic effects of anandamide using the Millar pressure-volume conductance catheter system. Baseline cardiovascular parameters, systolic and diastolic function at different preloads and baroreflex sensitivity were similar in FAAH-/- and FAAH+/+ mice. FAAH-/- mice displayed increased sensitivity to anandamide-induced, CB1-mediated, hypotension and decreased cardiac contractility compared to FAAH+/+ littermates. In contrast, the hypotensive potency of synthetic CB1 agonist HU210, and the level of expression of myocardial CB1 were similar in the two strains. The myocardial levels of anandamide and oleoylethanolamide, but not 2-arachidonylglycerol, were increased in FAAH-/- compared to FAAH+/+ mice. These results indicate that mice lacking FAAH have a normal hemodynamic profile, and their increased responsiveness to anandamide-induced hypotension and cardiodepression is due to the decreased degradation of anandamide rather than an increase in target organ sensitivity to CB1 agonists.




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