REGULATION OF FREE ARACHIDONIC-ACID LEVELS IN ISOLATED SALIVARY-GLANDS FROM THE LONE STAR TICK - A ROLE FOR DOPAMINE

An important regulatory step for prostaglandin synthesis is the availability of the precursor, free arachidonic acid (AA). In isolated salivary glands of the lone star tick, Amblyomma americanum (L.), the level of free AA appears to depend on higher phospholipase A(2) (PLA(2)) activity rather than decreased rates of re-esterification by lysophosphatide acyl transferase (LAT). This conclusion is supported by experiments where inhibition of LAT with merthiolate was without effect, while the calcium ionophore A23187, a PLA(2) stimulant, increased levels of free AA. The PLA(2) activity in A. americanum was reduced by the substrate analog, PLA(2) inhibitor, oleyloxyethyl phosphorylcholine in a dose-dependent manner, but was insensitive to the other mammalian PLA(2) inhibitors mepacrine (20 mu M), aristolochic acid (45 mu M), and dexamethasone (50 mu M). No substrate preference was observed for the functional group of the phospholipid, with phosphatidylcholine and phosphatidylethanolamine being equal sources of AA in A23187-stimulated glands. Compared to phospholipids containing other fatty acids, only arachidonyl-phospholipid (arachidonyl-PL) was significantly hydrolyzed by PLA(2) activity in A23187-stimulated glands. Dopamine was as effective as A23187 as a stimulant of PLA(2) activity in isolated glands, but this effect was abolished in the presence of the calcium channel blocking agent verapamil. It is concluded that free AA levels in tick salivary glands are increased through activation of a Type IV-like PLA(2) following an increase of intracellular calcium caused by the opening of voltage-dependent calcium channels due to dopamine stimulation. (C) 1995 Wiley-Liss, Inc.