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Direct dopamine D 2 ‐receptor‐mediated modulation of arachidonic acid release in transfected CHO cells without the concomitant administration of a Ca 2+ ‐mobilizing agent
Author(s) -
Nilsson Christer L,
Hellstrand Monika,
Ekman Agneta,
Eriksson Elias
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702025
Subject(s) - dopamine receptor d2 , chemistry , agonist , sulpiride , arachidonic acid , endocrinology , medicine , pharmacology , dopamine , receptor , biochemistry , antagonist , biology , enzyme
In CHO cells transfected with the rat dopamine D 2 receptor (long isoform), administration of dopamine per se elicited a concentration‐dependent increase in arachidonic acid (AA) release. The maximal effect was 197% of controls (EC 50 =25 n M ). The partial D 2 receptor agonist, (−)‐(3‐hydroxyphenyl)‐N‐ n ‐propylpiperidine [(−)‐3‐PPP], also induced AA release, but with somewhat lower efficacy (maximal effect: 165%; EC 50 =91 n M ). The AA‐releasing effect of dopamine was counteracted by pertussis toxin, by the inhibitor of intracellular Ca 2+ release, 8‐( N N ‐diethylamino)octyl‐3,4,5‐trimethoxybenzoate (TMB‐8), by excluding calcium from the medium, by the phospholipase A 2 (PLA 2 ) inhibitor, quinacrine, and by long‐term pretreatment with the phorbol ester, 12‐ O ‐tetradecanoylphorbol‐13‐acetate (TPA). In addition, it was antagonized by the D 2 antagonists, raclopride and (−)‐sulpiride–but not by (+)‐sulpiride–and absent in sham‐transfected CHO cells devoid of D 2 receptors. The results obtained contrast to the previous notion that dopamine and other D 2 receptor agonists require the concomitant administration of calcium‐mobilizing agents such as ATP, ionophore A‐23187 (calcimycin), thrombin, and TRH, to influence AA release from various cell lines.British Journal of Pharmacology (1998) 124 , 1651–1658; doi: 10.1038/sj.bjp.0702025