scholarly journals Membrane-associated forms of peptidylglycine alpha-amidating monooxygenase activity in rat pituitary. Tissue specificity.

1988 ◽  
Vol 263 (16) ◽  
pp. 7550-7554 ◽  
Author(s):  
V May ◽  
E I Cullen ◽  
K M Braas ◽  
B A Eipper
1983 ◽  
Vol 64 (2) ◽  
pp. 2P-3P
Author(s):  
R.D. Askew ◽  
D.B. Ramsden ◽  
H.C. Sheppard

Endocrinology ◽  
2002 ◽  
Vol 143 (11) ◽  
pp. 4330-4338 ◽  
Author(s):  
Lee Chapman ◽  
Aya Nishimura ◽  
Julia C. Buckingham ◽  
John F. Morris ◽  
Helen C. Christian

Abstract Our recent studies on rat pituitary tissue suggest that the annexin I-dependent inhibitory actions of glucocorticoids may not be exerted directly on endocrine cells but indirectly via folliculo-stellate (FS) cells. FS cells contain glucocorticoid receptors and abundant annexin I. We have studied the localization of annexin I in FS cells and the ability of dexamethasone to induce annexin I secretion by an FS (TtT/GF) cell line, using Western blotting and immunofluorescence microscopy. Exposure of TtT/GF cells to dexamethasone (0.1 μm, 3 h) caused an increase in the amount of annexin I protein in the intracellular compartment and attached to the surface of the cells. In nonpermeabilized cells, immunofluorescence labeling revealed that annexin I immunoreactivity was associated with the cell surface and concentrated in focal patches on the ends of cytoplasmic processes; dexamethasone (0.1 μm, 3 h) increased both the number and intensity of these foci. Immunogold electron microscopy confirmed in anterior pituitary tissue the presence of immunoreactive-annexin at the surface of FS cell processes contacting endocrine cells. These data support our hypothesis that annexin I is released by FS cells in response to glucocorticoids to mediate glucocorticoid inhibitory actions on pituitary hormone release via a juxtacrine mechanism.


1986 ◽  
Vol 43 (3) ◽  
pp. 336-339 ◽  
Author(s):  
Taiichiro Okajima ◽  
Georg Hertting

1986 ◽  
Vol 108 (3) ◽  
pp. 323-328 ◽  
Author(s):  
T. A. Bramley ◽  
G. S. Menzies ◽  
D. T. Baird

ABSTRACT The effects of a number of analogues of gonadotrophin-releasing hormone (GnRH) on the binding of a radiolabelled GnRH agonist (GnRH-A; d-Ser(But)6, des Gly10]GnRH-ethylamide) to homogenates of human corpus luteum (CL) and rat pituitary tissue were compared. Specific binding was inhibited by GnRH and GnRH-like peptides only. Both the C-terminal amide and N-terminal region of the GnRH molecule were required for binding in both tissues. However, amino acid substitutions at position 6 markedly enhanced, and at position 8 markedly reduced, binding potencies in rat pituitary tissue compared with human CL binding sites. These results indicate that GnRH-binding sites of rat pituitary and human luteal tissue have a similar degree of specificity for GnRH-like peptides, and a similar requirement for both N- and C-terminal regions of the peptide, but that differences in specificity related to the mid-chain region of GnRH exist between human luteal and rat pituitary binding sites. J. Endocr. (1985) 000, 000–000


1985 ◽  
Vol 106 (2) ◽  
pp. R5-R8 ◽  
Author(s):  
B.I. Baker ◽  
D.J. Bird ◽  
J.C. Buckingham

ABSTRACT Melanin-concentrating hormone (MCH) is a neural peptide associated with colour change in fishes. We show here that it also inhibits corticotrophin (ACTH) secretion. Synthetic salmonid MCH at a concentration of 100 pmol/l reduced the in-vitro release of ACTH by pars distales (pDs) taken from stressed trout. At lower concentrations (10 pmol/l) the peptide inhibited CRF-41-induced secretion of ACTH by pDs removed from unstressed trout, while at higher concentrations (10 nmol/l) it reduced the corticotrophic response of rat pituitary tissue to CRF-41.


1976 ◽  
Vol 68 (1) ◽  
pp. 89-94 ◽  
Author(s):  
M. SHAHMANESH ◽  
S. L. JEFFCOATE

SUMMARY Rat stalk median eminence (SME) extract was incubated with various quantities of an antiserum raised against synthetic luteinizing hormone releasing hormone (LH-RH) and the resulting material was used at two or more dose levels to stimulate release of LH and FSH from anterior pituitary tissue, obtained from male rats, incubated in vitro. The resulting dose–response lines were used to obtain the LH- and FSH-releasing potency of the material, expressed as a percentage of SME extract pre-incubated with normal rabbit serum. Treatment with various doses of antiserum reduced LH-releasing and FSH-releasing potencies to a similar extent. Stalk median eminence extract and synthetic LH-RH were incubated with antiserum and directly compared in the same experiment in vitro. The changes in LH and FSH release caused by pre-treatment with antibody were similar for SME extract and synthetic LH-RH. In a final experiment, SME extract was passed through a column of Sepharose 2B particles to which was coupled anti-LH-RH antibody. The resulting material, when mixed with synthetic LH-RH and used to stimulate rat pituitary tissue in vitro caused a similar increase in the LH- and FSH-releasing potencies of the synthetic decapeptide. It is concluded that rat SME extract contains a single releasing factor for LH and FSH immunologically indistinguishable from synthetic LH-RH.


1959 ◽  
Vol 19 (2) ◽  
pp. 164-173 ◽  
Author(s):  
L. MARTINI ◽  
A. DE POLI ◽  
A. PECILE ◽  
S. SAITO ◽  
F. TANI

SUMMARY It is shown that anterior pituitary tissue grafted into hypophysectomized rats and lacking any connexion with the median eminence does not retain any somatotrophic or gonadotrophic activities, but has some adrenocorticotrophic (ACTH) and thyrotrophic (TSH) activities. This conclusion is based on: (1) the partial maintenance of thyroid and adrenal weight; (2) the results of studies on 131I uptake and on TSH concentration in the grafted pituitaries; (3) the persistence of significant adrenocorticotrophic responses to Pitressin, lysine-vasopressin and Guillemin's fraction D; (4) the presence of histological and histochemical signs of activity in the grafted gland. The subnormal levels of secretion observed in the pituitary grafted into sites far removed from the sella turcica, seem to depend on the lack of some neurohumoral stimulus which normally activates the intact pituitary via the hypophysio-portal vessels. Evidence is given that vasopressin may be the hypothalamic neurohumor involved in ACTH secretion, and that the ACTH-releasing activity of Guillemin's fraction D may be accounted for by its vasopressin content.


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