CB1 receptors are expressed by human oesophageal epithelial cells and in Gastro-Esophageal Reflux Disease these receptors are downregulated (Calabrese et al., 2010).
CB2 receptors are found in the digestive tract (Salaga et al., 2017), however, they are not expressed in human esophageal epithelial cells (Calabrese et al., 2010).
In a study with mice, it was shown that CB2 receptor agonists in a dose-dependent manner exhibit a protective effect against ethanol and diclofenac-induced gastric ulcers. CB2 antagonists reversed this effect (Salaga et al., 2017).
It was found that in the myenteric plexus of the esophagus human CB1 and CB2 receptors are expressed abundantly (Rohof et al., 2012).
In mice, gastric acidity and ulceration can be reduced by increasing ambient endocannabinoid levels through blocking MAGL (Crowe and Kinsey, 2017).
In dogs and human volunteers, the number of Transient Lower Esophageal Sphincter Relaxations was reduced by THC. CB1 antagonist SR141716A blocked this effect, proposing participation of CB1 (Beaumont et al., 2009).