Wednesday November 25 2009 | Biotechnology feed | All feeds

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CB1 antagonists reduce survival rates following experimental myocardial infarction

The cloning of CB1 and CB2 cannabinoid receptor subtypes at the beginning of the last decade, and the subsequent development of selective tools has advanced the concept of therapeutically targeting the cannabinoid receptors. A wide range of clinical conditions are indicated, and since CB1 receptors are extensively expressed in the brain, many diseases suggested to benefit from cannabinoid ligands are those with a central components. Consequently CB1 receptor antagonists have been suggested to improve Parkinson's disease by regulating motor centers including the basal ganglia and to reduce food intake by acting at reward centers. 

Cannabinoid receptors are widespread and a host of physiological functions have been attributed to endogenous cannabinoids including the control of cardiovascular function being strong vasodilators as well as playing a role in the response to hemorrhage. The risk of CB1 antagonists carrying serious cardiovascular side-effects must therefore be closely investigated. Research emerging from the University of Wurzburg is important in this respect. In a model of myocardial infarction, the CB1 antagonist, SR141716A was found to prevent associated reduction mean arterial pressure. However, tachycardia and mortality were both doubled. This suggests that the safety of CB1 antagonists should be carefully monitored in patients at risk of myocardial infarction. 


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