title: [Effect of human inhibin alpha-fragments and monoaminergic neurotransmitters on progesterone(P4) production by corpus luteum(CL) of rat in vitro].
abstract: The effects of exogenenous monoaminergic neurotransmitters (norepinephrine, NE; epinephrine, E; dopamine, DA and 5-HT) and inhibin alpha N-terminal fragments P32 (1-32), P32-Tyr on P4 production by incubated rat CL cells were studied. The results demonstrated that: (1) alpha fragments caused significant inhibition on P4 production. (2) 0.1 mmol/L NE (or E) and 10 mumol/L DA produced a marked increase in both basal and hCG induced P4 production by CL cells (P < 0.001). The rank orders of potency of the catecholamines in stimulating P4 production were different, for basal P4 production, NE > E > DA; but for hCG induced P4 production, DA > E > NE, i.e. the order just reversed. Addition of P32-Tyr significantly neutrolized the stimulatory action of E, but only slightly increased the action of NE. (3) alpha receptor blocker phentolamine and beta receptor blocker propranolol were effective in decreasing basal and hCG-induced P4 production, the latter being more effective than the former. It was further shown that both blockers augmented the inhibitory effect of alpha-fragments on P4 production. (4) Unlike NE, E, and DA, 5-HT at 0.5 mumol/L exerted inhibitory effect on the basal and hCG-induced P4 production, but profoundly supressed the inhibitory effect of alpha-fragments on P4 production. The above results suggested: (1) Adrenergic, DA and 5-HT receptors are present in rat CL, where catecholamine might exert a stimulating effect on basal and hCG-induced P4 production via different pathways. (2) The inhibitory effect of P32, P32-Tyr on P4 production might be related to their inhibition by partial blocking alpha/beta receptors, which were antagnized by 5-HT. (3) The action of P32, P32-TYr on P4 production is brought on the participation of neurotransmitters NE, E, DA and 5-HT.
authors.affiliation: Department of Physiology, Harbin Medical University.
authors.forename: J H
authors.initials: JH
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Ni
authors.forename: C P
authors.initials: CP
authors.lastname: Cheng
authors.forename: Y
authors.initials: Y
authors.lastname: Sun
authors.forename: G C
authors.initials: GC
authors.lastname: Lu
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D006063:Chorionic Gonadotropin / Q000378:metabolism; D003338:Corpus Luteum / Q000378:metabolism*; D004298:Dopamine / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006801:Humans; D007265:Inhibins / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology*; D010446:Peptide Fragments / Q000494:pharmacology*; D011374:Progesterone / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D006063:Chorionic Gonadotropin; D010446:Peptide Fragments; D012701:Serotonin; D011374:Progesterone; D007265:Inhibins; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine