Psychologic and Neural Regulation of Growth Hormone Secretion

In order to determine whether or not there is a tonic dopamine (DA) control of GH release, the effect of an anti-dopaminergic agent, sulpiride, on GH secretion was studied in 12 normal subjects. After the administration of sulpiride, serum concentrations of sulpiride reached a peak value (1.93+0.1 µg/ml, mean+s.E.M., n=6) at 15 min and then showed a gradual decrease. Concomitantly, mean plasma prolactin (PRL) showed a rapid elevation, with a peak value of 161.9+11.5 ng/ml at 30 min, followed by a gradual decrease. Even at 180 min after sulpiride injection, the plasma PRL was still 9 times higher than the initial level (p<0.005). Within 90 min after the injection, 12 subjects showed a minimal but significant decrease in GH (from 0.78+0.17 to 0.32+0.03 ng/ml, p<0.02). After another 90 min, the plasma GH level increased and the mean peak value (8.1+2.7 ng/ml) at 180 min was significantly higher than the initial value (p<0.02). From these observations, it was suggested that sulpiride inhibited the endogenous DA activity over 180 min, and that the GH decrease within 90 min was due to a suppression of endogenous DA activity. Factors other than DA, however, might be considered for the GH increase after 90 min. dopamine; GH; prolactin; sulpiride It is well known that dopaminergic agonists, e.g. L-dopa, apomorphine, piribedil and CB-154, have stimulatory effects on GH secretion in man (Eddy et al. 1971;Lal et al. 1972;Camanni et al. 1975;Orsetti et al. 1978). In addition, it has been reported that dopamine (DA)-antagonists, e.g. pimozide and sulpiride, can inhibit the GH release induced by DA-agonists (Liuzzi et al. 1976;Lal et al. 1977; Mori et al. 1977). These findings suggest a role for DA in the release of GH. Effects produced by pharmacological doses of DA-agonists, however, do not necessarily imply that endogenous DA has a physiological role in the control of GH secretion. To test whether this is in fact the case, we examined the effect of a DAantagonist, sulpiride (Restelli et al. 1975;MacLeod and Robyn 1977). If there is a tonic DA control of GH release, sulpiride would be expected to block it with resultant changes in plasma GH.

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“…1,4,7,8,11,12). After the injection, all six cases showed dramatic elevations and gradual declines of the serum sulpiride levels (Fig.…”

Section: Resultsmentioning

confidence: 94%

Evidence for endogenous dopaminergic control of GH release in man.

Hanew

Sasaki

Yoshinaga

1981

Tohoku J. Exp. Med.

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“…Trotz durchschnittlich normaler Assimilations raten in Begleitung pathologischer Anderson-Kurven könnte an ein episodisch defektes "Assimilations-Filter" für peripher passierende glykolytische Gipfel gedacht werden. Dabei könnte der hochlabilen Wachstumshormon-Sekretion (HGH) eine bestimmende pathophysiologische Rolle zukommen (11). Die Regu lation der HGH-Sekretionsraten erscheint glucosespezifisch, alpha-adrenerge Stimulation fördert sie und hemmt sowohl die periphere Glucoseassimilation wie den intrazellulären Glucoseumsatz; alpha-adrenerge Blockade reduziert die HGHSekretion selbst bei insulininduzierter Hypoglykämie noch bis zu 50%, und BetaBlockade stimuliert sie entsprechend (unter anderem: 8, 9, 11, 24, 25, 33, 58, 59).…”

Section: Methoden Probanden Und Resultateunclassified

Pathologische Labilität venöser Nüchternblutzucker-Regulation in psychotischen Erkrankungen

Klempel¹,

Bleeker²

1979

Psychopathology

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The lability of peripheral venous postabsorptive blood sugar regulation was investigated in 98 patients suffering from floridly psychotic diseases (45 somatically based psychoses, 27 endogenous/involutional depressions, and 26 schizophrenic psychoses). In total, 259 times, in 30-sec intervals, 10 fasting blood sugar values each were determined (so-called ‘Anderson curves’). The maximal normal range of 36 mg% of spontaneous blood sugar oscillations in normal probands was exceeded in 17% of depressive, in 15% of schizophrenic, and in 12% of somatically based psychoses. The frequency and probability of appearance of pathological Anderson curves proved independent of any clinical-psychiatric diagnosis, and only significantly correlated with the criterion ‘psychotically ill’. Discussed are primary central deviations from nominal gluco-sensitive regulatory ‘tone’ as postulated cause of pathological lability of venous blood sugar homeostasis resulting. Besides additional, pre-known glucose-metabolic derangements accompanying certain neuro-psychiatric syndromes, pathological Anderson curves in psychotic illness are looked at as unspecific functional deviations involving bipolar-adrenergic dysbalances.

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“…(see reviews by Brown and Reichlin, 1972;Merimee and Rabin, 1973 ;Reichlin, 1974). In this connection it is of considerable interest that elevated HGH levels have been found during stages 3 and 4 sleep (Takahashi et ai, 1968) in which a relative rapid decline in arterial pressure (Coccagna et ai, 1971 ) and a consistent decrease in CBF with pronounced regional differences (Townsend et ai, 1973) have been described.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Hypoperfusion as a Stimulus for Growth Hormone Release in Man

Kellerová¹,

Vigaŝ²

1980

Horm Res

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In healthy male volunteers the effect of a short-term cerebral ischemia due to an acute orthostatic hypotension, on the release of growth hormone (HGH) was studied. Peroral administration of guanethidine 12.5 mg t.i.d. for 3 days plus 25 mg before the experiment was used to block peripheral vascular reflexes and thus to provoke orthostatic intolerance. An extreme increase of HGH serum levels (on average from 0.8 to 13.6 ng/ml; p < 0.001) was found in subjects who developed clinical signs of syncope after assuming upright posture. The possible mechanisms of this finding are discussed.

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Psychologic and Neural Regulation of Growth Hormone Secretion

Cited by 80 publications

References 39 publications

Evidence for endogenous dopaminergic control of GH release in man.

Evidence for endogenous dopaminergic control of GH release in man.

Pathologische Labilität venöser Nüchternblutzucker-Regulation in psychotischen Erkrankungen

Cerebral Hypoperfusion as a Stimulus for Growth Hormone Release in Man

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