Lack of evidence for impaired dopamine receptor function in experimental hepatic coma in the rabbit.
In order to determine whether hepatic coma is associated with an altered sensitivity of the dopamine (DA) receptor in the brain, the activity of DA-sensitive adenylate cyclase was assayed in homogenates from the corpus striatum of normal rabbits and rabbits with galactosamine-induced fulminant hepatic failure by measuring cyclic adenosine monophosphate production from adenosine triphosphosphate radioimmunochemically. The kinetic properties of adenylate cyclase in control rabbits and rabbits with hepatic coma were similar (Km, 17 +/- 2.9 (S.E.M.) vs 20 +/- 6.4 mM; Vmax, 816 +/- 58 vs 1054 +/- 233 pmol/mg protein/5 min, respectively). Hepatic coma was not associated with any changes in the responses of the DA receptor-adenylate cyclase system to DA (maximum stimulation 60% vs 57%), sodium fluoride (maximum stimulation 104% vs 132%), or a D-2 DA receptor agonist (maximum inhibition 18% vs 12%). These findings make it unlikely that alterations of dopaminergic neurotransmission play an important role in the pathogenesis of hepatic coma.
D000262:Adenylyl Cyclases / Q000378:metabolism*; D000818:Animals; D003342:Corpus Striatum / Q000201:enzymology / Q000502:physiology*; D005688:Galactosamine; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000201:enzymology / Q000503:physiopathology*; D007700:Kinetics; D011817:Rabbits; D011954:Receptors, Dopamine / Q000502:physiology*; D009435:Synaptic Transmission
D011954:Receptors, Dopamine; D005688:Galactosamine; D000262:Adenylyl Cyclases