Literature DB >> 2897995

Withdrawal of endogenous somatostatin induces secretion of growth hormone-releasing factor in rats.

N Miki1, M Ono, K Shizume.   

Abstract

Secretion of GH occurs in episodic bursts under the dual control of two hypothalamic peptides, GH-releasing factor (GRF) and GH-inhibiting factor (somatostatin, SRIF). Recent studies in rats suggest that episodic GH secretion is generated by the periodic release of GRF, which is associated with the simultaneous withdrawal of SRIF secretion. To test the possibility that GRF discharge is functionally coupled with the withdrawal of SRIF, we investigated whether acute withdrawal of SRIF can induce GRF release by the rat hypothalamus using highly specific antisera against SRIF and rat GRF. In conscious unrestrained rats, i.v. administration of SRIF antiserum at the period of the GH trough induced a rapid onset of the GH secretory surge with a peak value of 309 +/- 67 micrograms/l (mean +/- S.E.M.) 30 min after injection. Pretreatment with antiserum to rat GRF resulted in a approximately 83% suppression of the GH surge induced by SRIF antiserum without affecting the trough GH values. GRF antiserum also significantly inhibited the spontaneous GH surge. In urethane-anaesthetized rats, as in conscious rats, an acute phasic GH release was caused by SRIF antiserum despite the interference of anaesthesia with spontaneous GH secretion. A further surge-like GH secretion was not restored during the next several hours, however, with the GH secretory profile being characterized by a tonic increase in the baseline levels of GH. In the anaesthetized rat antiserum to rat GRF, having no effect on basal GH levels, similarly inhibited by approximately 66% the acute GH surge induced by SRIF antiserum and decreased by about 30% the later sustained rise in GH.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1988        PMID: 2897995     DOI: 10.1677/joe.0.1170245

Source DB:  PubMed          Journal:  J Endocrinol        ISSN: 0022-0795            Impact factor:   4.286


  6 in total

1.  Regulation of basal, pulsatile, and entropic (patterned) modes of GH secretion in a putatively low-somatostatin milieu in women.

Authors:  Johannes D Veldhuis; Susan A Hudson; Joy N Bailey; Dana Erickson
Journal:  Am J Physiol Endocrinol Metab       Date:  2009-06-02       Impact factor: 4.310

2.  Gender modulates sequential suppression and recovery of pulsatile growth hormone secretion by physiological feedback signals in young adults.

Authors:  Johannes D Veldhuis; Leon Farhy; Arthur L Weltman; Jonathan Kuipers; Judith Weltman; Laurie Wideman
Journal:  J Clin Endocrinol Metab       Date:  2005-02-22       Impact factor: 5.958

3.  Estradiol regulates GH-releasing peptide's interactions with GH-releasing hormone and somatostatin in postmenopausal women.

Authors:  Catalina Norman; Nanette L Rollene; Dana Erickson; John M Miles; Cyril Y Bowers; Johannes D Veldhuis
Journal:  Eur J Endocrinol       Date:  2013-11-29       Impact factor: 6.664

4.  Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

Authors:  N Miki; M Ono; N Hizuka; T Aoki; H Demura
Journal:  J Clin Invest       Date:  1992-07       Impact factor: 14.808

5.  Suppression of growth hormone (GH) secretion by a selective GH-releasing hormone (GHRH) antagonist. Direct evidence for involvement of endogenous GHRH in the generation of GH pulses.

Authors:  C A Jaffe; R D Friberg; A L Barkan
Journal:  J Clin Invest       Date:  1993-08       Impact factor: 14.808

6.  Endogenous growth hormone (GH)-releasing hormone is required for GH responses to pharmacological stimuli.

Authors:  C A Jaffe; R DeMott-Friberg; A L Barkan
Journal:  J Clin Invest       Date:  1996-02-15       Impact factor: 14.808

  6 in total

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