scholarly journals Blockade of endogenous growth hormone-releasing hormone receptors dissociates nocturnal growth hormone secretion and slow-wave sleep

2004 ◽  
pp. 561-566 ◽  
Author(s):  
SK Jessup ◽  
BA Malow ◽  
KV Symons ◽  
AL Barkan
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Hormone Receptors ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Nrem Sleep ◽  
Temporal Association ◽  
Sleep Stages ◽  
Sleep Study

OBJECTIVES: A temporal association between non-rapid eye movement (NREM) sleep stages 3 and 4 and nocturnal augmentation of GH release was found long ago, yet the precise mechanism for this association has not been identified. It has been shown, however that pulsatile GHRH administration increases both slow-wave sleep (SWS) and GH. Based on these data, a role for GHRH as an inducer of SWS was proposed. To test this hypothesis, we have performed the corollary experiment whereby the action of endogenous GHRH has been antagonized. DESIGN: Healthy men (20-33 years old) had an infusion of GHRH antagonist ((N-Ac-Tyr(1), D-Arg(2)) GHRH-29 (NH(2))) or saline for a 12-h period, between 2100 and 0900 h. An i.v. bolus of GHRH was given at 0700 h and GH samples were drawn from 0700 to 0900 h to document the efficacy of GH suppression by the GHRH antagonist. METHODS: A limited montage sleep study was recorded from 2300 to 0700 h during each admission. Plasma GH concentrations were analyzed by the use of a sensitive chemiluminometric assay. RESULTS: Effectiveness of the GHRH antagonist was validated in all subjects by demonstrating 93+/-1.8% (P=0.012) suppression of GH response to a GHRH bolus. Polysomnography demonstrated that the percentage of SWS was not different when saline and GHRH antagonist nights were compared (P=0.607); other quantifiable sleep parameters were also unchanged. CONCLUSIONS: We conclude that endogenous GHRH is indispensable for the nocturnal augmentation of GH secretion, but that it is unlikely to participate in the genesis of SWS.

Suppression of nocturnal growth hormone secretion in epilepsy with continuous spike-waves during slow-wave sleep

1999 ◽  
Vol 41 (2) ◽  
pp. 192-194 ◽  
Author(s):  
Kuniaki Iyoda ◽  
Hitoshi Tobiume ◽  
Susumu Kanzaki ◽  
Syouko Takano2 And Yoshiki Seino
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion

PHYSIOLOGICAL GROWTH HORMONE SECRETION DURING SLOW-WAVE SLEEP IN SHORT PREPUBERTAL CHILDREN

1987 ◽  
Vol 27 (3) ◽  
pp. 355-361 ◽  
Author(s):  
P. ADLARD ◽  
F. BUZI ◽  
J. JONES ◽  
R. STANHOPE ◽  
M. A. PREECE
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Prepubertal Children

STUDIES ON THE POSTPONED GROWTH HORMONE SECRETION FOLLOWING THE INFUSION OF SOMATOSTATIN

1976 ◽  
Vol 82 (2) ◽  
pp. 460-466 ◽  
Author(s):  
C. Lucke ◽  
B. Höffken ◽  
A. von zur Mühlen
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Rapid Rise ◽  
Trigger Mechanism ◽  
Gh Secretion ◽  
Inhibiting Factor ◽  
Rebound Phenomenon

ABSTRACT It is well known and also confirmed in this study that somatostatin (growth hormone inhibiting factor, GHIF) prevents the nocturnal GH secretion, as long as the peptide is infused. Following the infusion a rapid rise in GH levels is seen in sleeping subjects with peak values of 26.8 ± 9.7 ng/ml compared to 31.7 ± 4.7 ng/ml (± sem) in control nights. Delayed GH peaks were seen even in the absence of slow wave sleep. No postponed GH rise was observed when subjects fell asleep again. These data demonstrate that the postponed nocturnal GH peak does not represent a rebound phenomenon to a previous trigger mechanism but is acutely sleep induced.

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea

1987 ◽  
Vol 116 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Steven J. Goldstein ◽  
Richard H. K. Wu ◽  
Michael J. Thorpy ◽  
Robert J. Shprintzen ◽  
Robert E. Marion ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Obstructive Sleep

Abstract. Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (> 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

A reexamination of the relationship between growth hormone secretion and slow wave sleep using delta wave analysis

1990 ◽  
Vol 27 (5) ◽  
pp. 497-509 ◽  
Author(s):  
David B. Jarrett ◽  
Joel B. Greenhouse ◽  
Jean M. Miewald ◽  
Iva B. Fedorka ◽  
David J. Kupfer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Wave Analysis ◽  
Delta Wave ◽  
The Relationship

Sleep-endocrine effects of mifepristone and megestrol acetate in healthy men

1998 ◽  
Vol 274 (1) ◽  
pp. E139-E145 ◽  
Author(s):  
Klaus Wiedemann ◽  
Christoph J. Lauer ◽  
Margarete Hirschmann ◽  
Kristina Knaudt ◽  
Florian Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Sleep Eeg ◽  
Megestrol Acetate ◽  
Simultaneous Administration ◽  
Healthy Men ◽  
Eeg Recordings ◽  
Time Awake

Administration of steroid hormones was demonstrated to modulate the sleep electroencephalogram (EEG) and sleep-associated hormonal secretion in specific ways. The present study was conducted to compare the effects of mifepristone (Mif), a mixed glucocorticoid (GR) and progesterone receptor (PR) antagonist, and megestrol acetate (Meg), a PR agonist. Nine healthy men were pretreated with either placebo or 200 mg Mif or 320 mg Meg, or a combination of both. Changes in plasma adrenocorticotropic hormone (ACTH), cortisol, and growth hormone concentrations were registered every 30 min; sleep EEG recordings were obtained continuously. Administration of Mif increased the morning plasma ACTH and cortisol surges, whereas Meg had the opposite effect. Growth hormone secretion was lowered by Mif pretreatment and enhanced by Meg. Simultaneous administration of both compounds led to largely compensated effects. The sleep EEG changes induced by Mif were a slight increase in the time awake and a delayed onset of slow-wave sleep. Meg led to a reduction of rapid-eye-movement sleep. Simultaneous administration of Mif and Meg showed a synergism in increasing time awake and shallow sleep: it therefore may be concluded that the sleep EEG effects are mediated by an interaction of GR and PR in unknown mechanisms.

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls

1987 ◽  
Vol 116 (1) ◽  
pp. 36-42 ◽  
Author(s):  
A. Steiger ◽  
T. Herth ◽  
F. Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Cell Activity ◽  
Cortisol Concentration ◽  
Sleep Stages ◽  
Sleep Structure ◽  
Endocrine Activity ◽  
Normal Controls

Abstract. Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 ± 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

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