Faculty Opinions recommendation of Somatostatin dramatically stimulates growth hormone release from primate somatotrophs acting at low doses via somatostatin receptor 5 and cyclic AMP.

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.

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Interaction of Somatostatin Inhibition and Dibutyryl Cyclic AMP or Potassium Stimulation of Growth Hormone Release from Perifused Rat Pituitaries

Endocrinology ◽

10.1210/endo-101-4-1044 ◽

1977 ◽

Vol 101 (4) ◽

pp. 1044-1053 ◽

Cited By ~ 37

Author(s):

MAX E. STACHURA ◽

R. FITZER

Keyword(s):

Growth Hormone ◽

Cyclic Amp ◽

Hormone Release ◽

Growth Hormone Release ◽

Dibutyryl Cyclic Amp ◽

Potassium Stimulation ◽

Stimulation Of

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Altered release of growth hormone from dispersed adenohypophysial cells of streptozotocin diabetic rats. II. Effects of a phorbol ester and secretagogues which increase cyclic AMP

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y89-210 ◽

1989 ◽

Vol 67 (10) ◽

pp. 1321-1325

Author(s):

M. S. Sheppard ◽

B. A. Eatock ◽

R. M. Bala

Keyword(s):

Growth Hormone ◽

Cyclic Amp ◽

Phorbol Ester ◽

Phosphodiesterase Inhibitor ◽

Adenosine Monophosphate ◽

Diabetic Rats ◽

Hormone Release ◽

Growth Hormone Release ◽

Growth Hormone Releasing Factor ◽

Streptozotocin Diabetic Rats

We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. We have further studied the effects on growth hormone release from dispersed adenohypophysial cells of normal and streptozotocin diabetic rats of stimulation by compounds that increase cyclic 3′,5′-adenosine monophosphate formation or inhibit its breakdown and of a phorbol ester. The cells of the diabetic rats had no change in sensitivity in response to either cholera toxin or forskolin. A phosphodiesterase inhibitor caused an equal GH release from cells of both diabetic and normal animals after 60 min of incubation. There was no change in sensitivity of the cells of diabetic animals or in the maximal reponse of these cells to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate when compared with normal cells. A low calcium medium that blocked growth hormone releasing factor stimulated growth hormone release from normal rat cells also blocked it from the cells of the diabetic rats. These results suggest that the defect in response of the somatotrophs of diabetic animals is specific and only occurs with the hypothalamic hormones and not with other secretagogues.Key words: growth hormone, diabetes, streptozotocin, cyclic AMP, phorbol ester.

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Somatostatin receptor subtype 1 modulates basal inhibition of growth hormone release in somatotrophs

FEBS Letters ◽

10.1016/s0014-5793(99)01582-3 ◽

1999 ◽

Vol 462 (3) ◽

pp. 464-466 ◽

Cited By ~ 62

Author(s):

Hans-Jürgen Kreienkamp ◽

Ercan Akgün ◽

Hans Baumeister ◽

Wolfgang Meyerhof ◽

Dietmar Richter

Keyword(s):

Growth Hormone ◽

Somatostatin Receptor ◽

Receptor Subtype ◽

Hormone Release ◽

Growth Hormone Release ◽

Inhibition Of Growth

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Studies on growth hormone secretion: III. Inhibition of prostaglandin, theophylline and cyclic AMP stimulated growth hormone release by valinomycin in vitro

Biochemical and Biophysical Research Communications ◽

10.1016/0006-291x(71)90592-4 ◽

1971 ◽

Vol 44 (2) ◽

pp. 253-260 ◽

Cited By ~ 21

Author(s):

F. Hertelendy ◽

G. Peake ◽

H. Todd

Keyword(s):

Growth Hormone ◽

Cyclic Amp ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

Hormone Release ◽

Growth Hormone Release

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Requirement for adenosine triphosphate for stimulation in vivo of ox growth-hormone release

Biochemical Journal ◽

10.1042/bj1400479 ◽

1974 ◽

Vol 140 (3) ◽

pp. 479-485 ◽

Cited By ~ 2

Author(s):

Margaret McPherson ◽

J. George Schofield

Keyword(s):

Growth Hormone ◽

Cyclic Amp ◽

Prostaglandin E2 ◽

Adenosine Triphosphate ◽

Hormone Release ◽

Growth Hormone Release ◽

Atp Content ◽

Carbonyl Cyanide ◽

Stimulus Secretion Coupling

Rotenone, carbonyl cyanide chloromethoxyphenylhydrazone and 2,4-dinitrophenol cause parallel falls in ox pituitary ATP content and growth-hormone release in the presence of 65mm-K+. Carbonyl cyanide chloromethoxyphenylhydrazone (0.4μg/ml) prevented the rise in growth-hormone release, but not the rise in 3′:5′-cyclic AMP content after addition of prostaglandin E2 (1μg/ml). The rate of hormone release from unstimulated slices and from slices in the presence of Ba2+ at 2.3 or 6.9mm was proportional to the ATP content of the slices. Carbonyl cyanide chloromethoxyphenylhydrazone at concentrations that inhibited release in the presence of the three secretagogues did not alter the pituitary contents of Na+, K+ or Ca2+. The implications of these observations are discussed in terms of the mechanism of stimulus–secretion coupling.

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