Growth hormone secretion from chicken adenohypophyseal cells in primary culture: Effects of human pancreatic growth hormone-releasing factor, thyrotropin-releasing hormone, and somatostatin on growth hormone release

1987 ◽  
Vol 65 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Frank M. Perez ◽  
Sasha Malamed ◽  
Colin G. Scanes
Keyword(s):  
Growth Hormone ◽  
Primary Culture ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Factor ◽  
Pancreatic Growth ◽  
Culture Effects

Effect of epoxyeicosatrienoic acids on growth hormone release from somatotrophs

1989 ◽  
Vol 256 (2) ◽  
pp. E221-E226 ◽  
Author(s):  
G. D. Snyder ◽  
P. Yadagiri ◽  
J. R. Falck
Keyword(s):  
Growth Hormone ◽  
Arachidonic Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Epoxyeicosatrienoic Acids ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Epoxyeicosatrienoic Acid ◽  
Releasing Hormone

Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids. 5,6-Epoxyeicosatrienoic and 14,15-epoxyeicosatrienoic acid stimulated growth hormone release from an enriched population of somatotrophs (approximately 85%) by twofold. Inhibition of arachidonic acid metabolism by indomethacin did not affect growth hormone-releasing hormone stimulation of growth hormone release. In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release. 14,15-Epoxyeicosatrienoic acid stimulated a concentration-dependent increase (twofold) in the cytoplasmic concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the somatotrophs. 14,15-Epoxyeicosatrienoic acid also rapidly increased the intracellular free calcium concentration in somatotrophs from resting levels (approximately 80 nM) to greater than 250 nM. Growth hormone-releasing hormone increased the free intracellular calcium to 160-180 nM. Preincubation of somatotrophs with somatostatin inhibited growth hormone-releasing hormone-stimulated growth hormone secretion, cAMP accumulation, and 14,15-epoxyeicosatrienoic acid stimulated cAMP accumulation. These data are suggestive that the epoxyeicosatrienoic acids may have a role in the secretion of growth hormone.

Cycloheximide blocks insulin-like growth factor I but not somatostatin inhibition of growth hormone secretion

1987 ◽  
Vol 65 (4) ◽  
pp. 515-519 ◽  
Author(s):  
M. S. Sheppard ◽  
R. M. Bala
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Protein Synthesis Inhibitor ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Synthesis Inhibitor ◽  
Inhibition Of Growth ◽  
Igf I

Growth hormone secretion is controlled by the two hypothalamic hormones, growth hormone releasing factor (GRF) and somatostatin. In addition, the insulin-like growth factors (IGF or somatomedins) which are themselves growth hormone dependent, inhibit growth hormone release in vitro, therefore acting to close the negative feedback loop. The studies reported here examine some of the differences between inhibition of growth hormone secretion by somatostatin and IGF-I in vitro. The major finding is that cycloheximide, a protein synthesis inhibitor, blocks inhibition of GRF-stimulated growth hormone release caused by IGF-I, without changing the inhibition caused by somatostatin. The experiments were done by exposing mixed rat adenohypophysial cells to secretagogues with or without cycloheximide for 24 h in a short term culture. Somatostatin (0.6 nM) totally blocked rat GRF (1 nM) stimulated growth hormone release to values 48% of control (nonstimulated values), while IGF-1 (27 nM) only reduced the GRF-stimulated growth hormone release by 27 ± 3% (N = 5). Cycloheximide (15 μg/mL) totally blocked the effect of IGF-I but not somatostatin. A low concentration (0.12 nM) of somatostatin, which only partly inhibited growth hormone release, was also unaffected by cycloheximide. In purified rat somatotrophs, somatostatin (0.1 nM) inhibited GRF-stimulated cAMP levels slightly and reduced growth hormone release while IGF-I (40 nM) had no effect. We suggest that IGF-I inhibits only the secretion of newly synthesized growth hormone, while somatostatin inhibits both stored and newly synthesized growth hormone pools.

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