Here, I found this informative and interesting.....


Short answer:
Recent research suggests that various compounds in cannabis actively impede the production of saliva. It's not a sign of dehydration, simply a (mostly) harmless physiological response. Since this is due not to the heat caused by smoking cannabis, but is rather a physiological response to the compounds in marijuana, the method of ingestion doesn't make a difference.

Wanna know why? Read on

Most mammalian tissue contains two types of cannabinoid receptors, CB1 and CB2. CB1 receptors are found in nervous tissue (primarily in the brain, but also in other locations throughout the body) and CB2 receptors are found in hematopoietic cells and throughout the immune system (specifically in T cells, B cells, and macrophages.) Cannabis, as you likely know, contains THC (delta9-tetrahydrocannabinol). THC is a CB1 agonist. But THC isn't the only cannabinoid receptor agonist -- there are a number of other cannabinoids found in common marijuana, at least 66 have been discovered thus far. While the actions of these cannabinoids on CB1 and CB2 receptors are beyond the scope of this article, it can safely be assumed that there are likely more CB1/CB2 agonists in cannabis than just THC.
So how does this tie in to "cottonmouth"? Well as it turns out, the salivary system appears to respond to CB1 and CB2 agonists. In a study on the subject1, it was found that the submandibular glands of male rats contain CB1 and CB2 receptors. When researchers injected anandamide (an endocannabinoid with a high affinity for the CB1 and CB2 receptors) into rats' submandibular saliva glands, they found that it appeared to inhibit saliva production. The study concluded that anandamide "decreases saliva secretion in the SMG acting through CB1 and CB2 receptors."
Now while anandamide was chose by Prestifilipo et al., the inhibition of saliva production does not appear to be specific to anandamide. Instead, it is assumed that the activation of CB1 and CB2 in the submandibular gland was what caused the decrease in saliva production. If the inhibitory effect is indeed substance independent (i.e. not unique to the anandamide), then we might assume that any sufficiently strong CB1/CB2 agonist could cause a reduction in saliva production. Since marijuana contains a number of CB1 and CB2 agonists, and since CB1/CB2 agonists appear to have an effect on saliva production, it may well be that "cottonmouth" is due to the activation of CB1 and CB2 in saliva glands. Of course this conclusion is dependent on 1) the presence of CB1 and CB2 receptors in the saliva glands of humans 2) the presence of strong CB1 and CB2 agonists in recreationally-used marijuana and 3) human salivary secretion sharing certain similarities with the salivary secretion of rats.
Peace