Inhibition of adenosine 3′,5′-monophosphate accumulation in anterior pituitary gland in vitro by growth hormone-release inhibiting hormone

1974 ◽  
Vol 56 (4) ◽  
pp. 1052-1059 ◽  
Author(s):  
Pierre Borgeat ◽  
Fernand Labrie ◽  
Jacques Drouin ◽  
Alain Bélanger ◽  
Hans Immer ◽  
...  
1982 ◽  
Vol 2 (3) ◽  
pp. 147-154 ◽  
Author(s):  
R. Corder ◽  
J. E. C. Sykes ◽  
P. J. Lowry

Significant amounts of somatostatin-like immunor reactivity (SLI) were detected in the extract of a human catecholamine-secreting adrenal medullary tumour. After salt fractionation and reconstitution the major portion of SLI was purified by gel filtration and two HPLC steps; in all three systems it eluted in the position of somatostatin-14. The purified somatostatin-like peptide inhibited, in a dose-related manner, growth hormone release from stimulated perfused rat anterior pituitary ceils in vitro. Amino acid analysis showed the purified peptide to have an identical composition to somatostatin found in other species.


1985 ◽  
Vol 248 (4) ◽  
pp. E438-E442
Author(s):  
A. M. Judd ◽  
K. Koike ◽  
R. M. MacLeod

Arachidonate and its metabolites increase growth hormone release in vitro. A study was designed to determine whether arachidonate release from anterior pituitary cells is modified by growth hormone-releasing factor (GRF) or somatostatin (SRIF). Cultured pituitary cells were incubated with [3H]arachidonate to esterify the long-chain fatty acid into cellular lipids. The cells were extensively washed with medium containing no [3H]arachidonate and then incubated with GRF and/or SRIF for 30 min. The incubation medium was then extracted with ethyl acetate, and following thin-layer chromatographic separation, the radioactivity in the [3H]arachidonate band was measured. GRF in a concentration-dependent manner (1-30 nM) stimulated growth hormone and arachidonate release, whereas SRIF (100 nM) blocked the GRF-induced increase of growth hormone and arachidonate release. The effects of GRF on growth hormone and arachidonate were evident at time intervals as brief as 5 min. These findings support the hypothesis that arachidonate may play a role in the GRF-induced growth hormone release.


1983 ◽  
Vol 96 (3) ◽  
pp. 395-400 ◽  
Author(s):  
S. W. J. Lamberts ◽  
E. G. Bons ◽  
P. Uitterlinden ◽  
W. H. Hackeng

Cyproheptadine and its metabolite desmethylcyproheptadine were shown to suppress directly the release of adrenocorticotrophin (ACTH) and β-lipotrophin/β-endorphin activity from the neurointermediate lobe of the pituitary gland incubated in vitro. Neither compound affected the release of ACTH from the anterior pituitary gland. Serotonin stimulated the release of ACTH and β-lipotrophin/β-endorphin activity from the neurointermediate lobe, but did not influence the (desmethyl)cyproheptadine-mediated inhibition of hormone release. These results indicate that serotonin and cyproheptadine affect hormone release by the neurointermediate lobe by a direct action. The effect of cyproheptadine, however, might not be exerted by a serotonin receptor.


1989 ◽  
Vol 50 (5) ◽  
pp. 513-518 ◽  
Author(s):  
Robert Drouhault ◽  
Pierre Vacher ◽  
Jean P. David ◽  
Anne M. Courtes ◽  
Nidaravone Vilayleck ◽  
...  

1982 ◽  
Vol 92 (2) ◽  
pp. 303-308 ◽  
Author(s):  
T. R. HALL

Single pigeon anterior pituitary glands were incubated with or without a hypothalamus in media containing various drugs. Release of prolactin and growth hormone was quantified by an electrophoretic-densitometric method. The hypothalamus stimulated release of both prolactin and growth hormone from the pituitary gland. Dopamine did not affect hormone release from pituitary glands incubated alone, but inhibited hypothalamus-stimulated release of prolactin and augmented hypothalamus-stimulated release of growth hormone in a dose-related manner. The effects of dopamine were reversed by its antagonist, pimozide. Serotonin stimulated release of prolactin and inhibited release of growth hormone from pituitary–hypothalamus co-incubations, and these effects were blocked by its antagonist, methysergide. Thyrotrophin releasing hormone (TRH) stimulated release of both hormones directly from pituitary glands incubated alone. Dopamine now inhibited TRH-stimulated release of prolactin, without affecting TRH-stimulated release of growth hormone. These results indicate that the neurotransmitters, dopamine and serotonin, affect the in-vitro release of factors from the hypothalamus which control the secretion of prolactin and growth hormone. In addition, dopamine may inhibit release of prolactin directly from the pituitary gland, but only when secretion of prolactin is high initially.


1981 ◽  
Vol 59 (4) ◽  
pp. 307-310 ◽  
Author(s):  
Dominique Rouleau ◽  
Nicholas Barden

Rat anterior pituitary gland adenylyl cyclase activity is stimulated by prostaglandins with an order of potency of [Formula: see text] which is the same for cAMP accumulation and growth hormone release. Somatostatin inhibited prostaglandin-stimulated adenylyl cyclase with an ID50 of 1.48 × 10−8 ± 0.27 × 10−8 M. GTP also stimulated adenylyl cyclase activity at concentrations greater than 10−6 M but did not prevent inhibition by somatostatin. These results indicate that at least one action of somatostatin is exerted directly on cAMP formation.


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