To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Dopamine D(2) receptor-in… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Contact form


Note! If you want an answer on a question you must specify your email address

Dopamine D(2) receptor-induced COX-2-mediated production of prostaglandin E(2) in D(2)-transfected Chinese hamster ovary cells without simultaneous administration of a Ca(2+)-mobilizing agent.

Journal article
Authors Monika Hellstrand
Elias Eriksson
Christer Nilsson
Published in Biochemical pharmacology
Volume 63
Issue 12
Pages 2151-8
ISSN 0006-2952
Publication year 2002
Published at Institute of Physiology and Pharmacology, Dept of Pharmacology
Pages 2151-8
Language en
Keywords Animals, Arachidonic Acids, pharmacology, CHO Cells, Calcium, metabolism, Calcium Channel Blockers, pharmacology, Cricetinae, Cyclooxygenase 2, Dinoprostone, biosynthesis, Dopamine, pharmacology, Dopamine Antagonists, pharmacology, Drug Interactions, Enzyme Inhibitors, pharmacology, Gallic Acid, analogs & derivatives, pharmacology, Indomethacin, pharmacology, Isoenzymes, metabolism, Naphthalenes, pharmacology, Nitrobenzenes, pharmacology, Phosphatidylcholines, pharmacology, Prostaglandin-Endoperoxide Synthases, metabolism, Pyrones, pharmacology, Quinacrine, pharmacology, Receptors, Dopamine D2, genetics, metabolism, Salicylamides, pharmacology, Salicylates, pharmacology, Sulfonamides, pharmacology, Tetradecanoylphorbol Acetate, pharmacology, Transfection
Subject categories Pharmacology and Toxicology


We have earlier demonstrated that dopamine stimulates the liberation of the prostaglandin E(2) (PGE(2)) precursor, arachidonic acid, in Chinese hamster ovary cells transfected with the rat dopamine D(2) receptor (long isoform), also without concomitant administration of a Ca(2+)-releasing agent [Nilsson et al., Br J Pharmacol 1998;124:1651-8]. In the present report, we show that dopamine, under the same conditions, also induces a concentration-dependent increase in the production of PGE(2), with a maximal effect of 235% at approximately 100 microM, and with an EC(50) of 794 nM. The effect was counteracted by the D(2) antagonist eticlopride, pertussis toxin, the inhibitor of intracellular Ca(2+) release TMB-8, incubation in Ca(2+)-free experimental medium, and PKC desensitization obtained by chronic pretreatment with the phorbol ester TPA. It was also antagonized by the non-specific cyclooxygenase (COX) inhibitor, indomethacin, and by the selective COX-2 inhibitor, NS-398, but not by the specific COX-1 inhibitor, valeryl salicylate. Both the non-specific phospholipase A(2) inhibitor, quinacrine, and an inhibitor of cPLA(2) and iPLA(2), AACOF3, counteracted the effect; in contrast, a selective iPLA(2) inhibitor, BEL, and a selective sPLA(2) inhibitor, TAPC, were ineffective. No effects of dopamine were obtained in control cells mock-transfected with the p3C vector only. The results reinforce previous assumptions that dopamine may interact with eicosanoid metabolism by means of D(2) receptor activation, and implicate an involvement of cPLA(2) and COX-2 in this effect. It is suggested that measurement of dopamine-induced PGE(2) production may serve as a convenient way to study D(2) receptor function in vitro.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?