INACTIVATION OF SOMATOSTATIN BY PEPTIDASES IN DIFFERENT AREAS OF THE RAT BRAIN

1977 ◽  
Vol 85 (1) ◽  
pp. 1-10 ◽  
Author(s):  
E. C. Griffiths ◽  
S. L. Jeffcoate ◽  
D. T. Holland
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Male Rat ◽  
Peptidase Activity ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Brain Areas ◽  
Specific Radioimmunoassay ◽  
Optimum Ph ◽  
The Central Nervous System

ABSTRACT With the availability of a sensitive and specific radioimmunoassay for growth hormone-release-inhibiting hormone (somatostatin or GH-RIH), it has been possible to investigate the presence of peptidase enzymes capable of inactivating this hypothalamic hormone in the hypothalamus and other brain areas of the rat. It was found that both supernatant and particulate fractions from male rat hypothalami rapidly inactivated somatostatin and that the enzymes involved have an optimum pH of 7.3. Peptidase activity was significantly higher in the supernatant than in the particulate fraction from the hypothalamus, thalamus, cortex and cerebellum. Besides confirming the presence of peptidases inactivating the release-inhibiting hormone in the hypothalamus (the site of somatostatin synthesis and release), the results may indicate that somatostatin has a functional significance outside the hypothalamus-anterior pituitary axis but within the central nervous system.

Characterization of the somatostatin-like immunoreactivity extracted from an adrenal medullary tumour

1982 ◽  
Vol 2 (3) ◽  
pp. 147-154 ◽  
Author(s):  
R. Corder ◽  
J. E. C. Sykes ◽  
P. J. Lowry
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Gel Filtration ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Identical Composition ◽  
Salt Fractionation ◽  
Somatostatin 14

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.

scholarly journals Increase in pituitary adenosine 3′:5′-cyclic monophosphate content and potentiation of growth-hormone release from heifer anterior pituitary slices incubated in the presence of 3-isobutyl-1-methylxanthine

1974 ◽  
Vol 142 (2) ◽  
pp. 295-300 ◽  
Author(s):  
J. George Schofield ◽  
Margaret McPherson
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Prostaglandin E2 ◽  
Anterior Pituitary ◽  
Phosphodiesterase Inhibitor ◽  
Secretory Process ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Inhibitor Concentration ◽  
Stimulation Of

The release of growth hormone from heifer anterior pituitary slices and the cyclic AMP content of the slices were increased by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, both increases being related to inhibitor concentration over the range 0.1–1.0mm. Neither Ba2+(6.9 or 2.3mm), K+(72mm), nor p-chloromercuribenzoate (20μm) had any effect on pituitary cyclic AMP content over a 20min period. 3-Isobutyl-1-methylxanthine potentiated the release of growth hormone in response to Ba2+(2.3mm) and K+(24mm), but the degree of potentiation did not depend on inhibitor concentration in the same way as did tissue cyclic AMP content. 3-Isobutyl-1-methylxanthine decreased the concentration of K+required to give maximum stimulation of growth-hormone release, but did not significantly increase the maximum response to Ba2+. Growth-hormone release in the presence of prostaglandin E2 (1μm) was increased by 3-isobutyl-1-methylxanthine and was inhibited by the prostaglandin antagonist, 7-oxa-13-prostynoic acid, although this antagonist increased the pituitary cyclic AMP concentration and potentiated the prostaglandin E2-induced rise in cyclic AMP content. The stimulation of growth-hormone release by p-chloromercuribenzoate was not potentiated by 3-isobutyl-1-methylxanthine. The data suggest that Ba+and K+act at the same point in the secretory process as 3-isobutyl-1-methylxanthine, although by a different mechanism, and that p-chloromercuribenzoate has a different point of action.

Thymosin Fraction 5 Stimulates Prolactin and Growth Hormone Release from Anterior Pituitary Cellsin Vitro*

Endocrinology ◽  
1987 ◽  
Vol 121 (6) ◽  
pp. 2035-2043 ◽  
Author(s):  
BRYAN L. SPANGELO ◽  
ALLAN M. JUDD ◽  
PHILIP C. ROSS ◽  
IVAN S. LOGIN ◽  
W. DAVID JARVIS ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Release ◽  
Growth Hormone Release

GRF increases release of growth hormone and arachidonate from anterior pituitary cells

1985 ◽  
Vol 248 (4) ◽  
pp. E438-E442
Author(s):  
A. M. Judd ◽  
K. Koike ◽  
R. M. MacLeod
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Concentration Dependent Manner ◽  
Anterior Pituitary Cells ◽  
Arachidonate Release

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.

Beta-Adrenergic Stimulation of Growth Hormone Release from Perifused Rat Anterior Pituitary Cells

1983 ◽  
Vol 37 (6) ◽  
pp. 473-475 ◽  
Author(s):  
Susan N. Perkins ◽  
William S. Evans ◽  
Michael O. Thorner ◽  
Michael.J. Cronin
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Anterior Pituitary Cells ◽  
Stimulation Of
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