title: Acute changes in dopamine levels in rat adrenal glands after administration of dopamine receptor agonists and antagonists.
abstract: The study was aimed at in vivo pharmacological identification of the possible dopamine (DA) receptor(s) involved in changes of the DA level in rat adrenal glands. Previous work in this laboratory has shown that the DA level is largely controlled by the rate of catecholamine synthesis. The rats were killed by decapitation after various periods of drug administration and the catecholamine content of adrenal glands and forebrain was measured by high-performance liquid chromatography with electrochemical detection. Administration of the DA D-1 + D-2 receptor agonist, apomorphine, induced a statistically significant increase in DA levels in the adrenal glands. The same effect was noted after administration of the DA D-2 receptor agonist, quinpirole. The DA D-2 receptor antagonist, raclopride, blocked the apomorphine-induced increase in adrenal DA levels but had no effect per se on these levels. The DA D-1 receptor agonist, SKF 38393, and the DA D-1 receptor antagonist, SCH 23390, did not have any effect on apomorphine-induced changes in DA content in the adrenals. The DA elevating effect of the DA D-2 receptor agonist, quinpirole, in the adrenals was completely blocked by the DA D-2 receptor antagonist, domperidone. This compound does not cross the blood-brain barrier readily and is thus supposed to act mainly on peripheral tissues. In support of this, the dose of domperidone used did not affect brain DOPAC levels. Our data, together with observations reported in the literature, indicate that the adrenal medulla contains DA receptors of the D-2 subtype, which are capable of controlling the DA level in rat adrenal glands.
authors.affiliation: Department of Pharmacology, University of Göteborg, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Kujacic
authors.forename: K
authors.initials: K
authors.lastname: Svensson
authors.forename: L
authors.initials: L
authors.lastname: Löfberg
authors.forename: A
authors.initials: A
authors.lastname: Carlsson
mesh_terms: D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D015306:Biogenic Monoamines / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D003655:Decerebrate State; D004294:Domperidone / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism*; D015259:Dopamine Agents / Q000494:pharmacology*; D018492:Dopamine Antagonists; D004563:Electrochemistry; D004837:Epinephrine / Q000378:metabolism; D004873:Ergolines / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D019257:Quinpirole; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D015306:Biogenic Monoamines; D015259:Dopamine Agents; D018492:Dopamine Antagonists; D004873:Ergolines; D015102:3,4-Dihydroxyphenylacetic Acid; D019257:Quinpirole; D004294:Domperidone; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; D001058:Apomorphine; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine