Positive role of non-N-methyl-D-aspartate receptors in the control of growth hormone secretion in male rats

1996 ◽  
Vol 19 (6) ◽  
pp. 353-358 ◽  
Author(s):  
L. Pinilla ◽  
M. Tena-Sempere ◽  
D. Gonzalez ◽  
E. Aguilar
1995 ◽  
Vol 269 (4) ◽  
pp. E683-E690 ◽  
Author(s):  
J. P. Turner ◽  
G. S. Tannenbaum

Despite convincing evidence that somatostatin (SRIF) and growth hormone (GH)-releasing factor (GRF) individually play crucial roles in GH regulation, the nature of the interplay between these two hypothalamic hormones is far from clear. In the present study, we used the long-acting SRIF analogue, octreotide, as a probe in both the normal and mutant dwarf (dw) rat 1) to further elucidate the temporal nature of the SRIF-GRF interaction in vivo and 2) to define possible mechanisms of action of SRIF in generating pulsatile GH secretion. Normal free-moving adult male rats pretreated with octreotide (25 and 50 micrograms iv) and subsequently challenged with GRF (1 micrograms iv) exhibited a markedly blunted GH response to exogenous GRF 1 h after treatment. In contrast, preexposure to octreotide for 3 h produced a two- to threefold augmentation in GH responsiveness to GRF. Compared with normal saline-pretreated controls, 3-h pretreatment with octreotide produced a 14- to 16-fold augmentation in the postinhibitory rebound release of GH after the coadministration of native SRIF-14 and GRF (P < 0.001). In dw rats, which show a selective reduction in GH synthesis and storage, 3-h preexposure to octreotide failed to significantly alter GRF-induced GH release. These results demonstrate that, in the normal male rat, a 3-h period of exposure to the SRIF analogue octreotide is sufficient to enhance GH responsiveness to GRF. Our findings suggest that this effect is due to a SRIF-mediated buildup of pituitary GH stores in a readily releasable poo.(ABSTRACT TRUNCATED AT 250 WORDS)


Endocrine ◽  
2005 ◽  
Vol 28 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Enrique Aguilar ◽  
Manuel Tena-Sempere ◽  
Leonor Pinilla

2013 ◽  
Vol 80 (6) ◽  
pp. 381-389 ◽  
Author(s):  
Maria Consolata Miletta ◽  
Martin H. Schöni ◽  
Kristin Kernland ◽  
Primus E. Mullis ◽  
Vibor Petkovic

1992 ◽  
Vol 4 (1) ◽  
pp. 9-14 ◽  
Author(s):  
M. T. Bluet-Pajot ◽  
F. Mounier ◽  
D. Durand ◽  
C. Kordon ◽  
C. Llorens-Cortes ◽  
...  

1981 ◽  
Vol 59 (10) ◽  
pp. 1082-1088 ◽  
Author(s):  
G. R. Cooper ◽  
S. H. Shin

Somatostatin inhibits not only growth hormone secretion, but also the secretion of several other hormones. The role of somatostatin in prolactin (PRL) secretion has not been clearly demonstrated. The present study was undertaken to examine the effects of somatostatin on rat PRL secretion in several different circumstances where the circulating PRL level is elevated: (1) the estradiol primed intact male rat, (2) normal and (3) estradiol primed rats pretreated with pimozide, (4) normal and (5) estradiol primed hypophysectomized male rats with adenohypophyses grafted under the kidney capsule (HAG rat). Blood samples (70 μL) were taken every 2 min via an indwelling atrial cannula from conscious, unrestrained animals. In the estradiol primed intact rats, a bolus injection of somatostatin (10, 100, and 1000 μg/kg) lowered PRL levels in a dose-dependent manner. When the PRL concentration was elevated by the administration of pimozide (3 mg/kg), a dopaminergic receptor blocking agent, somatostatin was ineffective in decreasing plasma PRL concentration but the PRL concentration was lowered by somatostatin when the rat had been primed with estradiol. Somatostatin had no effect on the normal HAG rats, but lowered the plasma PRL concentration in the estradiol primed HAG rats. Since somatostatin inhibits PRL secretion only in the estradiol primed rats, it is suggested that estradiol priming creates a new environment, presumably via new or altered receptors, which can be inhibited by somatostatin.


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.


2009 ◽  
Vol 390 (4) ◽  
pp. 1377-1381 ◽  
Author(s):  
Yolanda Pazos ◽  
Carlos J.P. Álvarez ◽  
Jesús P. Camiña ◽  
Omar Al-Massadi ◽  
Luísa M. Seoane ◽  
...  

1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


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