STIMULATION OF GROWTH HORMONE SECRETION IN MONKEYS BY ADRENALIN, PITRESSIN AND ADENOSINE-3′5′-CYCLIC MONOPHOSPHORIC ACID (3′5′-AMP)

1968 ◽  
Vol 59 (3) ◽  
pp. 390-396 ◽  
Author(s):  
J. J. Gagliardino ◽  
J. M. Martin

ABSTRACT Serum growth hormone (GH) levels were measured by immunoassay in anaesthetized, non-fasted female Rhesus monkeys. Adrenalin and Pitressin® administration significantly stimulated growth hormone secretion. I. v. injection of adenosine-3′5′-cyclic monophosphoric acid (3′5′-AMP) mimicked the stimulatory action of both adrenalin and Pitressin. The stimulation of GH secretion by 3′5′-AMP was blocked by dihydroergotamine. These results suggest that the effect of either adrenalin or Pitressin or both on GH secretion is mediated by the adenyl-cyclase – cyclic AMP system. The additional observation that Pitressin depresses at the same time the release of insulin may indicate that the adenyl-cyclase – cyclic AMP system acts as a common intermediate in the growth hormone-insulin balance.

1984 ◽  
Vol 4 (12) ◽  
pp. 995-1000 ◽  
Author(s):  
Janet E. Merritt ◽  
Pauline R. M. Dobson ◽  
Richard J. H. Wojcikiewicz ◽  
John G. Baird ◽  
Barry L. Brown

A possible role for Ca 2+ and calmodulin in the action of growth-hormone-releasing factor (GHRF) was investigated. Low extracellular Ca2+ (<100 μM), methoxyverapamil, flunarizine, cinnarizine, and Co2+ decreased both basal and GHRF-stimulated growth-hormone secretion, but did not totally inhibit GHRF-stimulation secretion. A calmodulin antagonist, W7, abolished GHRF-stimulated GH secretion, with no effect on basal secretion. It is suggested that GHRF may act primarily by elevating cellular cyclic AMP, which may then modulate calcium mobilization or flux; the increased intracellular Ca2+ concentrations may then activate calmodulin.


1986 ◽  
Vol 108 (3) ◽  
pp. 413-416 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
J. Rivier ◽  
W. Vale

ABSTRACT Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0·1 and 10 μg/kg, increased plasma GH concentrations in immature domestic fowl 5–10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 μg rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1–32) and (Nle27)-rhGRF(1–29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl. J. Endocr. (1986) 108, 413–416


2018 ◽  
Vol 237 (2) ◽  
pp. 165-173 ◽  
Author(s):  
J T Smith ◽  
A Roseweir ◽  
M Millar ◽  
I J Clarke ◽  
R P Millar

Kisspeptin signalling is indispensable for fertility, stimulating gonadotropin-releasing hormone (GnRH) secretion and mediating gonadal steroid feedback on GnRH neurons. Moreover, kisspeptin neurons have been implicated in other non-reproductive neuroendocrine roles. Kisspeptin appears to also regulate growth hormone secretion but much of the data appear contradictory. We sought to clarify a potential role of kisspeptin in growth hormone (GH) regulation by examining the effect of kisspeptin antagonists on GH secretion in ewes under various physiological conditions. Our data show clear and robust increases in GH secretion following lateral ventricle or third ventricle infusion of kisspeptin antagonists p-234 and p-271 in either ovariectomized or anestrous ewes. Central infusion of kisspeptin-10 had no effect on GH secretion. To determine the level at which kisspeptin may influence GH secretion, we examined expression of the cognate kisspeptin receptor, GPR54, in pituitary cells and showed by immunocytochemistry that the majority of somatotropes express GPR54 while expression was largely negative in other pituitary cells. Overall, we have demonstrated that blocking kisspeptin signalling by antagonists stimulates GH secretion in ewes and that this is likely mediated by inhibiting endogenous kisspeptin activation of GPR54 expressed on somatotropes. The findings suggest that endogenous kisspeptin inhibits GH secretion through GPR54 expressed on somatotropes.


Science ◽  
1969 ◽  
Vol 163 (3868) ◽  
pp. 705-705
Author(s):  
Lawrence A. Frohman ◽  
Lee L. Bernardis ◽  
Kenneth J. Kant

Science ◽  
1968 ◽  
Vol 162 (3853) ◽  
pp. 580-582 ◽  
Author(s):  
L. A. Frohman ◽  
L. L. Bernardis ◽  
k. J. Kant

Endocrinology ◽  
1973 ◽  
Vol 92 (5) ◽  
pp. 1349-1353 ◽  
Author(s):  
M. ZAKARIJA ◽  
J. M. MC KENZIE ◽  
C. H. BASTOMSKY

1971 ◽  
Vol 51 (3) ◽  
pp. 473-481 ◽  
Author(s):  
H. M. LLOYD ◽  
J. D. MEARES ◽  
JOAN JACOBI ◽  
FRANCES J. THOMAS

SUMMARY A single 12 mg dose of stilboestrol dipropionate given to 100-day-old male rats resulted in increased pituitary mitotic activity, pituitary weight and serum growth hormone; the latter rose from a mean value of 20 ng/ml to a maximum of 342 ng/ml 9 days later. Serum growth hormone and pituitary mitotic activity then gradually diminished but were still slightly increased on day 28. Serum growth hormone and pituitary weight were significantly correlated during the periods of rapidly rising and of sustained high levels of serum growth hormone. Indices of mitotic activity were correlated with serum growth hormone during the periods of rapidly rising and of falling levels of serum growth hormone.


1989 ◽  
Vol 4 (2) ◽  
pp. 135-138 ◽  
Author(s):  
Hameen Markar ◽  
John Bennie ◽  
Sheena Carroll ◽  
Ann Chiswick ◽  
Helen Wilson ◽  
...  

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1648-1653 ◽  
Author(s):  
Philippe Zizzari ◽  
Romaine Longchamps ◽  
Jacques Epelbaum ◽  
Marie Thérèse Bluet-Pajot

Administration of ghrelin, an endogenous ligand for the GH secretagogue receptor 1a (GHSR 1a), induces potent stimulating effects on GH secretion and food intake. However, more than 7 yr after its discovery, the role of endogenous ghrelin remains elusive. Recently, a second peptide, obestatin, also generated from proteolytic cleavage of preproghrelin has been identified. This peptide inhibits food intake and gastrointestinal motility but does not modify in vitro GH release from pituitary cells. In this study, we have reinvestigated obestatin functions by measuring plasma ghrelin and obestatin levels in a period of spontaneous feeding in ad libitum-fed and 24-h fasted mice. Whereas fasting resulted in elevated ghrelin levels, obestatin levels were significantly reduced. Exogenous obestatin per se did not modify food intake in fasted and fed mice. However, it inhibited ghrelin orexigenic effect that were evident in fed mice only. The effects of obestatin on GH secretion were monitored in superfused pituitary explants and in freely moving rats. Obestatin was only effective in vivo to inhibit ghrelin stimulation of GH levels. Finally, the relationship between octanoylated ghrelin, obestatin, and GH secretions was evaluated by iterative blood sampling every 20 min during 6 h in freely moving adult male rats. The half-life of exogenous obestatin (10 μg iv) in plasma was about 22 min. Plasma obestatin levels exhibited an ultradian pulsatility with a frequency slightly lower than octanoylated ghrelin and GH. Ghrelin and obestatin levels were not strictly correlated. In conclusion, these results show that obestatin, like ghrelin, is secreted in a pulsatile manner and that in some conditions; obestatin can modulate exogenous ghrelin action. It remains to be determined whether obestatin modulates endogenous ghrelin actions.


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