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Y Furuki

Publications and source records attributed to Y Furuki.

27 records · Page 2Linked to original sources
PubMed1985

[The effects of dopamine on the release of immunoreactive beta-endorphin-like peptide from the dispersed cells of the rat neurointermediate lobe].

The intermediate lobe of the rat pituitary gland is a homogeneous population of cells which synthesize and secrete various peptides related to ACTH and lipotropin derived from a common precursor, proopiomelanocortin. Catecholamine beta-receptor (beta-adrenoceptor) and dopamine receptor which are present in the intact cells of the intermediate lobe, remain functional in the enzymatically dispersed cells. In this study we investigated the mechanism by which beta-endorphin is released from the dispersed cells of the neurointermediate lobe of the rat pituitary gland. 1-Isoproterenol stimulated the release of immunoreactive beta-endorphin-like peptide (IR-beta-Ep) and the accumulation of adenosine 3', 5'-monophosphate (cAMP). On the other hand, dopaminergic drugs, apomorphine, bromocriptine, dopamine, lergotrile and lisuride, decreased the rate of release of IR-beta-Ep. Dopamine also inhibited the stimulatory effects of 1-isoproterenol on the release of IR-beta-Ep and cAMP accumulation. Dopamine antagonists, fluphenazine and sulpiride, diminished the inhibitory effects of dopamine on the release of IR-beta-Ep and cAMP accumulation which were stimulated by 1-isoproterenol. it has been reported that cholera toxin enhanced the release of IR-beta-Ep and the accumulation of cAMP in the rat neurointermediate lobe. After preincubation in the incubation medium containing 30 nM cholera toxin for 2 hours, the cells (CT cells) showed spontaneous release of IR-beta-Ep and cAMP accumulation. 1-Isoproterenol had no effect on the release of IR-beta-Ep and cAMP accumulation in CT cells. Dopamine, however, inhibited both the release of IR-beta-Ep from CT cells and cAMP accumulation in CT cells. These results suggest that dopamine may be involved in the regulatory mechanism of IR-beta-Ep release from the dispersed cells of the rat neurointermediate lobe.

Animals↗
PubMed1985

Involvement of calcium in the release of immunoreactive beta-endorphin-like peptide from dispersed cells of the neurointermediate lobe of the rat pituitary gland.

The presence of Ca2+ in the incubation medium was required for stimulation of the release of the immunoreactive beta-endorphin-like peptide (IR-beta-EP) from the dispersed cells of the neurointermediate lobe of rat pituitary gland by adenosine 3',5'-monophosphate (cAMP) analogs, a phosphodiesterase inhibitor, L-isoproterenol, cholera toxin and forskolin. The basal release observed in the absence of the stimulants was also dependent on the addition of Ca2+. A calcium antagonist (verapamil) inhibited the effects of the stimulants. A calcium ionophore (A23187) enhanced the release of IR-beta-EP, but did not stimulate the formation of cAMP. These findings suggest that Ca2+ has the essential role in the release of beta-endorphin from the neurointermediate lobe of rat pituitary gland.

1-Methyl-3-isobutylxanthine↗
PubMed1985

In vivo and in vitro studies on the production of placental proteins (human chorionic gonadotropin, human placental lactogen, and pregnancy-specific beta 1-glycoprotein) in an adrenal choriocarcinoma.

The ectopic production of placental proteins (human chorionic gonadotropin [hCG], human placental lactogen, and pregnancy-specific beta 1-glycoprotein) by an adrenal choriocarcinoma was investigated experimentally in vivo and in vitro. By an immunohistochemical method, the choriocarcinoma tissues obtained from the right adrenalectomy were found to react with hCG, human placental lactogen, and pregnancy-specific beta 1-glycoprotein antibodies. The concentrations of hCG-beta, human placental lactogen, and pregnancy-specific beta 1-glycoprotein in the tumor fluid were 1480, 100, and 47 ng/mL, respectively. On incubation of the tumor slices in vitro, the concentration of hCG-beta in the incubation medium increased markedly with time. Serial sections of the removed uterus and right ovary did not reveal any primary trophoblastic lesions. The present tumor responded well to double chemotherapy with actinomycin D and methotrexate, resulting in a decrease of the level of serum hCG-beta to less than 10 ng/mL after four courses of the chemotherapy.

Adrenal Gland Neoplasms↗
PubMed1984

[The effects of cholera toxin in the release of beta-endorphin from the dispersed cells of the rat neurointermediate lobe].

The intermediate lobe cells of pituitary gland synthesize and secrete bioactive peptides derived from proopiomelanocortin. In the present study, we investigated the effects of cholera toxin on the release of beta-endorphin (beta-Ep) from dispersed-intermediate lobe cells of rats. Cholera toxin added into culture medium, enhanced the intracellular accumulation of adenosine 3', 5'-monophosphate (cAMP) and the release of beta-endorphin like immunoreactive substance (beta-END-LIS). A positive dose-response relationship existed between the concentration of cholera toxin and the release of beta-END-LIS or the accumulation of cAMP. Maximal response was obtained with approximately 3 X 10(-10) M (in beta-END-LIS release) and 1 X 10(-9) M (in cAMP accumulation) concentration of cholera toxin. Incubation with cholera toxin (3 X 10(-8) M) resulted in a significant rise of cAMP accumulation after 20-30 min, and a 2-2.5 fold increase of beta-END-LIS release occurred after 60 min in comparison with nontreated cells. cAMP analog and phosphodiesterase inhibitor also increased the beta-END-LIS release). These results suggested the close relationship between cAMP accumulation and its biological effect (i.e. beta-END-LIS release).

Animals↗
PubMed1984

[Endocrine profile and electron microscopic study of ovarian androblastoma].

The endocrine profile of a 23-year-old woman with an androblastoma of the right ovary and the results of electron microscopic observation of the tumor are presented. The calculated ratio of testosterone in testosterone intraoperative peripheral vein blood, right ovarian vein blood, and right ovarian tumor fluid was 1:1.4:4.0. The peripheral levels of hormones before right salpingo-oophorectomy were testosterone, 6.26 ng/ml; dehydroepiandrosterone, 17.80 ng/ml; androstenedione, 1.61 ng/ml; and cortisol, 16.5 micrograms/ml, and the corresponding levels at 14 days after surgery were 0.50 ng/ml; 13.80 ng/ml; 1.27 ng/ml; and 15.2 micrograms/ml, respectively. The tumor was responsive to hCG, resulting in a marked increase in the serum concentrations of testosterone, androstenedione, and dehydroepiandrosterone (3.7 times, 5.3 times, and 2.4 times, respectively). Preoperatively, an elevated basal level of luteinizing hormone (LH) and a normal basal level of follicle-stimulating hormone (FSH) (high LH:FSH ratio, 6.6) were found. The electron microscopic findings for the tumor revealed Leydig cells, Sertoli cells, transitional cells with features of both Sertoli cells and Leydig cells, and dark cells. The dark cells had features similar to dark cells of normal ovarian stroma.

Adult↗
PubMed1983

[Mechanism of beta-endorphin release regulation--evaluation using dispersed cells of the pituitary intermediate lobe].

The intermediate lobe of the rat pituitary gland is a homogeneous population of cells synthesizing and secreting various peptides related to ACTH and lipotropin derived from a common glycoprotein precursor, pro-opiocortin. The release mechanism of beta-endorphin from the pituitary gland has been reported by a few investigators, but the precise mechanism is still unknown. The receptors for a catecholamine present in the intact intermediate lobe of the rat pituitary gland remain functional on the enzymatically dispersed cells which secrete beta-endorphin-like immunoreactivity (beta-EPLI) and synthesize adenosine-3',5'-monophosphate (cAMP). Stimulation of beta-adrenoceptor with 1-isoproterenol enhances the synthesis of cAMP and accelerates the rate of beta-EPLI release. The ability of beta-adrenergic agonists to enhance the synthesis of cAMP appears to be causally related to the physiological response to beta-adrenergic agonists (i.e. enhanced beta-EPLI release). Phosphodiesterase inhibitors (theophylline, 3-isobutyl-1-methyl xanthine), cAMP analogs (dibutyryl-cAMP, 8-bromo-cAMP) and cholera toxin also increase beta-EPLI release. These findings suggest that cAMP may participate in this beta-EPLI release process. Furthermore, dopamine inhibits basal beta-EPLI release and also diminishes l-isoproterenol stimulated beta-EPLI release.

Animals↗