title: Pharmacological characterization of the ergot alkaloid receptor in the salivary gland of the ixodid tick Amblyomma hebraeum.
abstract: Female ticks of the family Ixodidae osmoregulate by secreting the excess fluid of the blood meal back into the host's circulation via the salivary glands. At least three receptors control salivary fluid secretion in the tick Amblyomma hebraeum: (1) dopamine (DA) stimulates fluid secretion via a DA receptor, (2) ergot alkaloids (ErAs) stimulate fluid secretion via an ErA-sensitive receptor (the natural ligand of which has not been identified), and (3) a GABA receptor potentiates the action of DA and ErAs. Here we present some pharmacological properties of the ErA-sensitive receptor. Of the 11 ErAs we tested, (i) four were complete agonists (approximate concentration eliciting 50% maximum response is given in parentheses): dihydroergotamine (0.02 micromol l(-1)), ergonovine (ErN; 0.06 micromol l(-1)), methylergonovine (0.1 micromol l(-1)) and alpha-ergocriptine (0.9 micromol l(-1)); (ii) three were ;incomplete agonists' (approximate concentration eliciting 20% maximum response is given in parentheses): ergocorninine (3.5 micromol l(-1)), ergocristinine (7.5 micromol l(-1)) and ergocristine (10 micromol l(-1)); (C) three were partial agonists (approximate concentration eliciting the respective maximum response in parentheses): ergocornine (50% maximum by 1 micromol l(-1)), methysergide (28% maximum by 10 micromol l(-1)) and bromocriptine (22% maximum by 10 micromol l(-1)); and (D) one had no activity up to 1 mmol l(-1): ergothioneine. Bromocriptine and methysergide did not antagonize the action of DA, but were effective competitive antagonists of ErN, with K(i)s of approximately 0.3 micromol l(-1) and 11 micromol l(-1), respectively. Ergothioneine was not an antagonist at either the DA- or ErA-sensitive receptor. The putative protein kinase C activators, 1-oleoyl-2-acetyl-sn-glycerol (OAG) and 1,2-dioctanoyl-sn-glycerol (DiC8), neither stimulated salivary fluid secretion nor potentiated the action of DA or ErN. The putative protein kinase C inhibitors, bisindolymaleimide (BIM) and calphostin C did not inhibit the action of DA or ErN, although low concentrations of calphostin C (10 nmol l(-1)) appeared to potentiate the action of DA but not ErN. The ion transport inhibitors, furosemide and amiloride (both up to 1 mmol l(-1)), had no significant effect on DA-stimulated or ErN-stimulated fluid secretion.
authors.affiliation: Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada. reuben.kaufman@ualberta.ca
authors.forename: W Reuben
authors.initials: WR
authors.lastname: Kaufman
authors.forename: Jessi L
authors.initials: JL
authors.lastname: Minion
mesh_terms: D000818:Animals; D004876:Ergot Alkaloids / Q000737:chemistry / Q000494:pharmacology*; D017136:Ion Transport / Q000187:drug effects; D026863:Ixodidae / Q000187:drug effects / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D011956:Receptors, Cell Surface / Q000819:agonists* / Q000037:antagonists & inhibitors*; D012463:Saliva / Q000378:metabolism; D012469:Salivary Glands / Q000187:drug effects / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D004876:Ergot Alkaloids; D011956:Receptors, Cell Surface; D011493:Protein Kinase C