Central Nervous System and Pituitary Mechanisms in Dopaminergic Stimulation of Growth Hormone Release in Women

1981 ◽  
Vol 32 (4) ◽  
pp. 213-216 ◽  
Author(s):  
Carlo Ferrari ◽  
Roberto Caldara ◽  
Cristiano Barbieri ◽  
Paolo Testori ◽  
Rosanna Benco ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Growth Hormone ◽  
Nervous System ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Dopaminergic Stimulation ◽  
Stimulation Of

l-Ornithine stimulates growth hormone release in a manner dependent on the ghrelin system

2017 ◽  
Vol 8 (6) ◽  
pp. 2110-2114 ◽  
Author(s):  
Yee Yin Ho ◽  
Junya Nakato ◽  
Takafumi Mizushige ◽  
Ryuhei Kanamoto ◽  
Mamoru Tanida ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
System P ◽  
Stimulation Of

Stimulation of growth hormone release induced by intraduodenally administered l-ornithine was mediated by the ghrelin system in rats.

scholarly journals INSULIN STIMULATION OF GROWTH HORMONE RELEASE. 574

1996 ◽  
Vol 39 ◽  
pp. 98-98 ◽  
Author(s):  
Janine E Sanchez ◽  
Jose Perez-Rodriguez ◽  
William W Cleveland
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Insulin Stimulation ◽  
Stimulation Of

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.

THE STIMULATION OF GROWTH HORMONE RELEASE BY ACTH AND ITS INHIBITION BY SOMATOSTATIN

1976 ◽  
Vol 81 (2) ◽  
pp. 263-269 ◽  
Author(s):  
J. Köbberling ◽  
H. Jüppner ◽  
R. D. Hesch
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Control Test ◽  
Plasma Growth Hormone ◽  
Normal Volunteers ◽  
Rapid Injection ◽  
Distinct Increase ◽  
Stimulation Of

ABSTRACT The rapid injection of 0.5 or 1.0 mg of tetracosactid (Synacthen®) was followed by a distinct increase of plasma growth hormone (GH) within 30 or 45 min in 5 of 7 normal volunteers. A second control test was performed in 3 of the 5 "responders" and 1 "non-responder" and showed a consistent reaction in all of them. The tests were then repeated in the 5 "responders" during an infusion of somatostatin (150 μg/h) and the GH response was totally abolished (3 subjects) or markedly reduced (2 subjects). Thus the ACTH induced GH release behaves in a manner similar to most other physiological or pharmacological stimuli of GH release. The cortisol output after ACTH was not altered by somatostatin.

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