The Diurnal Pattern of Plasma Growth Hormone Concentration in Children and Adolescents

Hunter, W. M.; Rigal, W. M.

doi:10.1677/joe.0.0340147

Cited by 89 publications

(25 citation statements)

References 8 publications

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“…In the six control studies carried out on the four male subjects, the plasma GH concentration, after the initial GH peak, remained at 5 mpg/ml or less for the remainder of the night except for one study in subject T. F. in which a secondary rise to 6 mpg/ml was noted. In the female subjects, with the exception of subject F. R. noted below, at least one and in some instances two subsequent GH peaks ranging from [8][9][10][11][12][13][14][15][16][17][18][19][20] mpg/ml were regularly observed. The peaks were usually sharply defined and limited in duration with return to basal levels (< 5 mpg/ml) before subse- the initial plasma GH peak was: always considerably greater than the subsequent elevated level.…”

Section: Resultsmentioning

confidence: 99%

Growth hormone secretion during sleep

Takahashi¹,

Kipnis²,

Daughaday³

1968

J. Clin. Invest.

760

268

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Plasma growth hormone (GH), insulin, cortisol, and glucose were measured during sleep on 38 nights in eight young adults. Blood was drawn from an indwelling catheter at 30-min intervals; EEG and electrooculogram were recorded throughout the night. In seven subjects, a plasma GH peak (13-72 mug/ml) lasting 1.5-3.5 hr appeared with the onset of deep sleep. Smaller GH peaks (6-14 mug/ml) occasionally appeared during subsequent deep sleep phases. Peak GH secretion was delayed if the onset of sleep was delayed. Subjects who were awakened for 2-3 hr and allowed to return to sleep exhibited another peak of GH secretion (14-46 mjug/ml). Peak GH secretion was not correlated with changes in plasma glucose, insulin, and cortisol. The effects of 6-CNS-active drugs on sleep-related GH secretion were investigated. Imipramine (50 mg) completely abolished GH peaks in two of four subjects, whereas chlorpromazine (30 mg), phenobarbital (97 mg), diphenylhydantoin (90 mg), chlordiazepoxide (20 mg), and isocarboxazid (30 mg) .did not inhibit GH peaks. Altered hypothalamic activity associated with initiation of sleep results in a major peak of growth hormone secretion unrelated to hypoglycemia or changes in cortisol and insulin secretion.

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Section: Resultsmentioning

confidence: 99%

Growth hormone secretion during sleep

Takahashi¹,

Kipnis²,

Daughaday³

1968

J. Clin. Invest.

760

268

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“…The effects of NE infusion on GH release have apparently not been studied in human adolescents. The similarity between the frequent episodic release of GH in human adolescents [Finkelstein et al, 1972;H unter and Rigal, 1966] and the recently de scribed four-hourly oscillatory release of GH in adolescent baboons [Stewart et al, 1977], suggests that the baboon may be an excellent experimental model for studies of GH regulation in the human adolescent.…”

Section: Discussionmentioning

confidence: 97%

Noradrenergic and Dopaminergic Regulation of GH and Prolactin in Baboons

Steiner¹,

Illner²,

Rolfs³

et al. 1978

Neuroendocrinology

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Aminergic regulation of growth hormone (GH) and prolactin (Prl) was studied in male adolescent baboons by i.v. infusion of dopamine (DA), norepinephrine (NE), thyrotropin-releasing hormone (TRH), phentolamine, haloperidol, and inhibitors of DA-β-hydroxylase and peripheral decarboxylase. 20-min infusion of DA (40 µg/kg·min) and 60-min infusion of NE (0.4 µg/kg·min) stimulated GH release. The DA-induced GH release was suppressed by concomitant infusion of FLA 63 (inhibitor of NE synthesis from DA) and by phentolamine, indicating α-adrenergic mediation of GH release. Micro-injection of DA (0.8 µg/kg) into the medial basal hypothalamus (MBH) lowered basal GH. Prl was released by i.v. TRH, and this effect was suppressed by i.v. DA but not by i.v. NE. Blockade of peripheral decarboxylase by carbidopa elicited a marked and sustained rise in Prl which was inhibited by i.v. DA. Microinjection of NE (0.8 µg/kg) into the MBH released Prl. These data indicate that in the MBH, α-adrenergic mechanisms release GH and Prl, and that dopaminergic mechanisms suppress GH.

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“…Scheving & Pauly (1966), Hunter & Rigal (1966), Dixit & Buckley (1967) and Krieger & Krieger (1967) observed circadian rhythms of a number of blood hormones in the rat. Min, Jones & Flink (1966) and Bahorsky & Bernardis (1967) demonstrated circadian rhythmicity in the renal excretion of magnesium, calcium, sodium, phosphorus and potassium and also indicated cyclic changes for many key metabolites in fasting and nonfasting rats.…”

Section: Introductionmentioning

confidence: 96%

Rat brain amines, blood histamine and glucose levels in relationship to circadian changes in sleep induced by pentobarbitone sodium

Friedman¹,

Walker²

1969

The Journal of Physiology

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1. The circadian patterns for onset and duration of sleep after the administration of a constant dose of pentobarbitone sodium have been measured in rats adapted to and maintained under a fixed illumination cycle. The relationship of these patterns to others for rectal temperature and motor activity as well as for noradrenaline (NA), 5‐hydroxytryptamine (5‐HT) and histamine in mid‐brain and caudate nucleus, and histamine and glucose in blood serum, has been examined. 2. The onset of sleep is longest and duration shortest during the phase of the illumination cycle when motor activity and rectal temperature are maximal. An inverse relationship for these parameters is found during the light phase of the illumination cycle. 3. In untreated rats, mid‐brain NA and histamine and caudate nucleus histamine levels are maximal and 5‐HT minimal during the dark phase of the illumination cycle. An inverse relationship for these parameters is found during the light phase of the illumination cycle. 4. Pentobarbitone sodium treatment significantly elevates mid‐brain NA and histamine and caudate nucleus histamine levels during the dark phase of the illumination cycle. Although 5‐HT levels are reduced over the entire circadian cycle this change is significant only during the light phase of the illumination cycle. 5. Pentobarbitone sodium treatment reverses the circadian pattern for body temperature, producing a mirror image of the control pattern. 6. The circadian pattern for blood serum histamine levels differs from the C.N.S. pattern for histamine. Peak levels occur at the end of the light phase of the illumination cycle. After pentobarbitone sodium these levels are reduced, although the circadian pattern is similar to the control. 7. Circadian blood glucose patterns have bimodal peaks; a primary peak at the end of the dark phase, a secondary peak at the end of the light phase of the illumination cycle. Pentobarbitone sodium did not significantly alter the pattern. The relationship between this pattern and C.N.S. and peripheral histamine and catechol amines is discussed.

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The Diurnal Pattern of Plasma Growth Hormone Concentration in Children and Adolescents

Cited by 89 publications

References 8 publications

Growth hormone secretion during sleep

Growth hormone secretion during sleep

Noradrenergic and Dopaminergic Regulation of GH and Prolactin in Baboons

Rat brain amines, blood histamine and glucose levels in relationship to circadian changes in sleep induced by pentobarbitone sodium

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