Enhancement of estradiol-induced DNA synthesis in the anterior pituitary gland by the peripheral-type benzodiazepine receptor ligand RO 5-4864

1986 ◽  
Vol 66 (3-4) ◽  
pp. 303-307 ◽  
Author(s):  
H. Stepie? ◽  
J. Kunert-Radek ◽  
M. Pawlikowski
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Benzodiazepine Receptor ◽  
Anterior Pituitary Gland ◽  
Receptor Ligand ◽  
Peripheral Type

Hyperprolactinaemia and DNA synthesis in the pituitary gland of the rat

1983 ◽  
Vol 97 (1) ◽  
pp. 65-74 ◽  
Author(s):  
J. A. Burdman ◽  
M. T. Calabrese ◽  
R. M. MacLeod
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Dopamine Receptor ◽  
Dna Content ◽  
Anterior Pituitary ◽  
Blocking Agent ◽  
Anterior Pituitary Gland ◽  
Host Animal ◽  
Receptor Blocking ◽  
Tumour Bearing

Hyperprolactinaemia produced in rats by the transplanted prolactin-secreting tumours MtTW15 and 7315a significantly (P<0·01) inhibited by 70% the incorporation of [3H]thymidine into the pituitary DNA of the host animals. The weight and the DNA content of the glands were significantly (P<0·01) reduced by 30%. The administration of haloperidol, a dopamine receptor blocking agent, to the tumour-bearing rats increased the suppressed DNA replication in the anterior pituitary glands by approximately 560% in the MtTW15-bearing rat and by 100% in the 7315a-bearing animals. Furthermore, injection of drugs which stimulate prolactin release either by blocking the synthesis of dopamine (α-methyl-p-tyrosine) or the re-uptake of dopamine (reserpine) stimulated DNA synthesis by 800 and 100% respectively in the anterior pituitary gland of rats bearing the MtTW15 tumour. In contrast, lisuride, a dopamine agonist, significantly inhibited the incorporation of [3H]thymidine into the DNA of the pituitary gland of normal but not hyperprolactinaemic rats. Chronically administered oestrogens to hyperprolactinaemic rats increased the weight (100%), DNA content (31%), incorporation of [3H]thymidine into DNA (680%) and synthesis and release of prolactin (300%) in the pituitary gland. The incorporation of [3H]thymidine into tumour DNA was several times higher than in the pituitary gland of the host animal and was not significantly modified by any of the above treatments. Likewise the hyperprolactinaemia of the tumour-bearing rats was not significantly changed. In conclusion, we have shown that hyperprolactinaemia inhibits DNA synthesis in the anterior pituitary gland and this inhibition can be reversed completely by a dopamine receptor blocking agent and by hypothalamic dopamine depleting drugs. We propose that dopamine regulates, either directly or indirectly, DNA synthesis in the lactotrophs of the pituitary gland, which may be responsive to negative feedback mechanisms.

Indomethacin inhibits the estrogen-induced DNA synthesis in the rat anterior pituitary gland

1981 ◽  
Vol 101 (3) ◽  
pp. 1052-1056 ◽  
Author(s):  
Marek Pawlikowski ◽  
Jolanta Kunert-Radek ◽  
Andrzej Lewiński ◽  
Ewa Karasek
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland

scholarly journals Purification of Dipeptidyl Aminopeptidase II (Dipeptidyl Arylamidase II) of the Anterior Pituitary Gland

1968 ◽  
Vol 243 (15) ◽  
pp. 4143-4150 ◽  
Author(s):  
J K McDonald ◽  
F H Leibach ◽  
R E Grindeland ◽  
S Ellis
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Dipeptidyl Aminopeptidase

scholarly journals Inhibition of glucose-induced insulin secretion by a peripheral-type benzodiazepine receptor ligand (PK 11195)

2000 ◽  
Vol 362 (1) ◽  
pp. 46-51
Author(s):  
Didier Pujalte ◽  
Sophie Claeysen ◽  
Samuel Dietz ◽  
Jeannie Chapal ◽  
Dominique Hillaire-Buys ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Benzodiazepine Receptor ◽  
Receptor Ligand ◽  
Peripheral Type

Effects of estrogens on the characteristics of [3H]spiroperidol and [3H]RU24213 binding in rat anterior pituitary gland and brain

1979 ◽  
Vol 16 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thérèse Di Paolo ◽  
Réjean Carmichael ◽  
Fernand Labrie ◽  
Jean-Pierre Raynaud
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland

Effect of hypothalamic neuropeptides on corticotrophin release from quarters of rat anterior pituitary gland in vitro

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Anterior Pituitary Gland ◽  
High Concentration ◽  
Response Curves ◽  
Corticotrophin Releasing Factor ◽  
Basal Release

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226

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