Studies on growth hormone secretion VIII effects of α,β-methylene-ATP on prostaglandin induced GH release and cyclic AMP accumulation in rat anterior pituitary glands

1976 ◽  
Vol 11 (2) ◽  
pp. 285-291
Author(s):  
Frank Hertelendy ◽  
Mary Yeh
1984 ◽  
Vol 107 (1) ◽  
pp. 36-41 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick

Abstract. Anterior pituitary glands from chickens (Gallus domesticus) were incubated with or without single, mediobasal chicken hypothalami in medium containing histamine, alone or together with the antagonist diphenhydramine or in medium containing gamma-aminobutyric acid (GABA), alone or together with the antagonists bicuculline or picrotoxin. The release of prolactin (Prl) and growth hormone (GH) was measured by homologous radioimmunoassay. Histamine had no direct effect on the release of either hormone but stimulated Prl (in a dose-related way) and GH release when anterior pituitary glands were co-incubated with hypothalami. Diphenhydramine also had no direct effect on Prl or GH secretion but blocked the stimulatory effect of histamine on hypothalamusinduced Prl and GH release. When anterior pituitary glands were incubated without hypothalami, GABA, bicuculline and picrotoxin had no effect on the release of Prl or GH. However, GABA inhibited the release of both hormones in a concentration-related manner, when anterior pituitary glands were co-incubated with hypothalami. This inhibition was blocked by both bicuculline and picrotoxin. These results suggest that histamine and GABA may be involved in controlling the secretion of Prl and GH from the avian pituitary gland, possibly by modifying the secretion of hypothalamic releasing and/or release-inhibiting hormones.


1982 ◽  
Vol 94 (2) ◽  
pp. 257-NP ◽  
Author(s):  
Marianne Hall ◽  
S. L. Howell ◽  
D. Schulster ◽  
M. Wallis

We have used fractionation on density gradients of Percoll to separate the cell types in the rat anterior pituitary gland and to produce a purified preparation of somatotrophs. The method differs from those described previously which used, for example, albumin or Ficoll gradients, in being more rapid and avoiding low temperatures, and therefore gives cells with improved viability. Anterior pituitary glands from male rats were dispersed with trypsin to produce 1·5 × 106–2·0 × 106 cells/gland. These were fractionated on hyperbolic density gradients of Percoll. Two bands of cells containing somatotrophs were detected, one of which (band A; density 1·075–1·082 g/cm3) contained approximately 90% somatotrophs, whereas the other (band B; density 1·055–1·068 g/cm3) contained about 70% somatotrophs mixed with other cells, especially lactotrophs. Cells in band A appeared more responsive to secretagogues than those in band B; growth hormone secretion was stimulated markedly by cyclic AMP derivatives and prostaglandin E2, and inhibited by somatostatin. Such purified somatotrophs are well suited to biochemical studies on the mechanism of the control of growth hormone secretion.


1979 ◽  
Vol 80 (2) ◽  
pp. 203-213 ◽  
Author(s):  
P. W. YOUNG ◽  
R. J. BICKNELL ◽  
J. G. SCHOFIELD

Acetylcholine (25 μmol/l) in the presence of the choline esterase inhibitor physostigmine (67 μmol/l) increased the release of growth hormone and efflux of 45Ca2+ from perifused bovine pituitary slices; the time taken for the maximal response to occur was the same. In batch incubations, acetylcholine (1 μmol/l–1 mmol/l) increased pituitary cyclic GMP concentrations in the pituitary gland within 2 min, and increased incorporation of [3H]inositol and [32P]phosphate into pituitary phosphatidyl inositol within 15 min. Cyclic AMP concentrations were not significantly changed 2 or 5 min after acetylcholine addition. All the tissue responses were inhibited by prior exposure of the tissue to atropine (1 μmol/l) but not by tubocurarine (10 μmol/l–1 mmol/l), indicating that the responses were mediated by receptors of the muscarinic type. The similarities between these responses and those to known hypothalamic hypophysiotrophic hormones are discussed.


2010 ◽  
Vol 10 (4) ◽  
pp. 541-545
Author(s):  
Masayoshi Arisawa ◽  
Tsunehisa Makino ◽  
Nobuhiro Uchida ◽  
Takashi Nagai ◽  
Shun-ichiro Izumi ◽  
...  

1987 ◽  
Vol 253 (5) ◽  
pp. E591-E594
Author(s):  
C. Schofl ◽  
J. Sandow ◽  
W. Knepel

The effect of human growth hormone-releasing factor (GRF) on intracellular free calcium concentration ([Ca2+]i) was examined in rat anterior pituitary cells. The [Ca2+]i was monitored directly by means of the intracellularly trapped fluorescent indicator, fura-2. GRF rapidly elevated [Ca2+]i, reaching a new plateau within approximately 30 s. The half-maximally effective concentration of GRF was approximately 130 pM. GRF produced a maximal increase in [Ca2+]i by approximately 120 nM. The GRF (2 nM)-induced elevation of [Ca2+]i was abolished by removal of extracellular calcium (Ca2+ omitted, 2 mM EGTA). The GRF (2 nM)-caused rise in [Ca2+]i was largely reduced in the presence of the calcium channel blockers Mg2+ (31.2 mM) or nifedipine (1 microM). An increase in [Ca2+]i by approximately 60 nM was elicited by the addition of prostaglandin E2 (1 microM), which can stimulate growth hormone secretion independent of GRF receptors. These data indicate that GRF elevates the [Ca2+]i, possibly in somatotrophs; this GRF-induced increase in [Ca2+]i may depend on an influx of extracellular Ca2+, largely through Mg2+- and nifedipine-sensitive calcium channels.


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