title: Evidence for a pathological reduction in brain dopamine metabolism in idiopathic hyperprolactinemia.
abstract: The role of brain catecholamine activity in the neuroendocrine regulation of the dopamine-PRL system in idiopathic hyperprolactinemia was investigated by high-performance liquid chromatography with electrochemical detector. We measured urinary dopamine, norepinephrine, epinephrine, vanillylmandelic acid, homovanillic acid, 3,4-dihydroxyphenylacetic acid and total 3-methoxy-4-hydroxyphenylglycol levels in 12 women with idiopathic hyperprolactinemia before and during either peripheral dopa-decarboxylase blockade, by carbidopa, or dopamine beta-hydroxylase blockade, by disulfiram. Homovanillic acid and 3,4-dihydroxyphenylacetic acid concentrations were significantly lower (p less than 0.001 and p less than 0.005, respectively) in patients with idiopathic hyperprolactinemia compared with those in 12 control subjects in the early follicular phase, whereas they were similar to those in the control subjects in the pre-ovulatory phase. Dopamine, norepinephrine, epinephrine, vanillylmandelic acid and 3-methoxy-4-hydroxyphenylglycol concentrations were similar to those of the control subjects in both phases of the cycle. During carbidopa administration the levels of all urinary catecholamines and metabolites were unchanged, except that of dopamine which dropped remarkably (p less than 0.001). During disulfiram administration dopamine, homovanillic acid and 3,4-dihydroxyphenylacetic acid concentrations increased (p less than 0.05, p less than 0.001 and p less than 0.005, respectively) and those of norepinephrine, vanillylmandelic acid and 3-methoxy-4-hydroxyphenylglycol decreased (p less than 0.05, p less than 0.001 and p less than 0.005, respectively), whereas epinephrine levels remained unaltered. These data support the existence of a quantitatively reduced brain dopamine activity in idiopathic hyperprolactinemia.
authors.affiliation: Institute of Reproductive Physiology and Pathology, S. Orsola Hospital, University Alma Mater Studiorum, Bologna, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Paradisi
authors.forename: G
authors.initials: G
authors.lastname: Grossi
authors.forename: A
authors.initials: A
authors.lastname: Pintore
authors.forename: S
authors.initials: S
authors.lastname: Venturoli
authors.forename: E
authors.initials: E
authors.lastname: Porcu
authors.forename: M
authors.initials: M
authors.lastname: Capelli
authors.forename: C
authors.initials: C
authors.lastname: Flamigni
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000652:urine; D000328:Adult; D001921:Brain / Q000378:metabolism*; D002230:Carbidopa / Q000494:pharmacology; D002851:Chromatography, High Pressure Liquid; D004221:Disulfiram / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism*; D004299:Dopamine beta-Hydroxylase / Q000502:physiology; D004837:Epinephrine / Q000652:urine; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D006719:Homovanillic Acid / Q000652:urine; D006801:Humans; D006966:Hyperprolactinemia / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000097:blood; D008734:Methoxyhydroxyphenylglycol / Q000652:urine; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D014642:Vanilmandelic Acid / Q000652:urine
chemical_list: D015102:3,4-Dihydroxyphenylacetic Acid; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D008734:Methoxyhydroxyphenylglycol; D014642:Vanilmandelic Acid; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D004299:Dopamine beta-Hydroxylase; D002230:Carbidopa; D004221:Disulfiram; D004298:Dopamine; D009638:Norepinephrine; D006719:Homovanillic Acid; D004837:Epinephrine