Abstract
Δ-Tetrahydrocannabinol (Δ 9-THC), the principal psychoactive constituent of Cannabis sativa, was found to increase glucagon activation of liver plasma membrane adenylate cyclase. In the presence of 30μM Δ 9-THC, the EC 50 for glucagon was decreased by 60% from 7.6 nM to 3.1 nM. 11-OH-Δ 9-THC, a psychoactive metabolite of Δ 9-THC, also increased glucagon activation of adenylate cyclase while two cannabinoids without marihuana-like psychoactive potency, cannabinol and cannabidiol, did not. At 30 μM, Δ 9-THC either slightly decreased or had no effect on the activation of adenylate cyclase by GTP, Gpp(NH)p, fluoride ion, forskolin or ATP alone. Δ 9-THC had no effect on the binding of [ 125I] glucagon to liver plasma membranes. Arrhenius plots demonstrated that Δ 9-THC and 11-OH-Δ 9-THC, but not CBD, decreased the activation energy above the break temperature. Therefore, Δ 9-THC increased the coupling of the glucagon receptor to adenylate cyclase apparently by removing a constraint on receptor- N s coupling.
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