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  • Title: Relationship between delta-9-tetrahydrocannabinol-induced arachidonic acid release and secretagogue-evoked phosphoinositide breakdown and Ca2+ mobilization of exocrine pancreas.
    Author: Chaudhry A, Thompson RH, Rubin RP, Laychock SG.
    Journal: Mol Pharmacol; 1988 Oct; 34(4):543-8. PubMed ID: 2459592.
    Abstract:
    We have previously shown that addition of exogenous arachidonic acid to pancreatic acinar cells inhibits the incorporation of myo-[3H]inositol into membrane phosphoinositides and causes a reduction in the steady state levels of [32P]phosphatidylinositol-4,5-bisphosphate (PtdIns4,5P2). In the present study, delta-9-tetrahydrocannabinol (THC) was utilized to raise endogenous levels of arachidonic acid. In acinar cells simultaneously prelabeled with [3H]arachidonic acid and [32P]Pi, THC (1-20 microM) produced a concentration-dependent increase in free [3H]arachidonic acid release and a reduction in the steady state levels of [32P]Ptd-Ins4,5P2. THC (1-20 microM) also caused a concentration-dependent inhibition of myo-[3H]inositol trisphosphate accumulation, cytoplasmic Ca2+ level, and amylase secretion elicited by 0.1 microM caerulein. The findings that THC (20 microM) was unable to inhibit either the rise in [Ca2+]i elicited by ionomycin, or the secretory response to phorbol myristic acid or ionomycin, indicate that THC exerts a selective inhibitory effect on the phosphoinositide messenger system. These results support the postulate that endogenous arachidonic acid serves as a negative feedback regulator of phosphoinositide turnover in exocrine pancreas.
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