A specific prostaglandin E2 receptor and its role in modulating salivary secretion in the female tick, Amblyomma americanum (L.).

Prostaglandins of the 2-series (e.g. PGE2) are typically synthesized from arachidonic acid (AA) after AA is released from cellular phospholipids after activation of an intracellular phospholipase A2 (PLA2). Treatment of isolated salivary glands with PLA2 inhibitor oleyloxyethyl phosphorylcholine (OPC) or prostaglandin synthetase inhibitors reduced dopamine-induced fluid secretion and cyclic AMP (cAMP) levels in isolated salivary glands. PGE2 and its analog, 17-phenyl trinor PGE2, partly reversed the inhibition of secretion and cAMP level by OPC, suggesting that prostaglandins may have an autocrine effect in modulating tick salivary gland function. A specific PGE2 receptor was identified in the plasma membrane fraction of the salivary glands. The receptor exhibits a single, high affinity PGE2 binding site with a KD approximately 29 nM, is saturable, reversible, and specific for PGE2 and coupled to a cholera toxin-sensitive guanine nucleotide regulatory protein. Assay of adenylate cyclase activity in salivary gland membranes showed that PGE2 neither stimulated nor inhibited adenylate cyclase activity, indicating that the PGE2 effects on cAMP levels and possibly secretion are indirect, and that the PGE2 receptor stimulates an alternate "second messenger" pathway.