TRH and Dopamine Interactions Affecting Pituitary Hormone Secretion

Burrow, Gerard N.; May, Philip B.; Spaulding, Stephen W.; Donabedian, R. K.

doi:10.1210/jcem-45-1-65

Cited by 154 publications

(51 citation statements)

References 26 publications

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“…Two groups of investigators have reported a modest but statistically significant rise when 3-7 pAg/kg min were given to a total of 12 normal subjects (12,13), but three other groups, using similar dosages, found no discernible effect in a total of 27 subjects (9-11). These discrepant results may be explained by the During the second period of exercise, the heart rate was increased to 150 beats/min by a work load of 752+66 kg/min in the normals and 625+94 in the diabetics (NS); oxygen consumption was 2,157±199 and 1,963±169 ml/min (NS).…”

Section: Discussionmentioning

confidence: 99%

Increased growth hormone response to dopamine infusion in insulin-dependent diabetic subjects: indication of possible blood-brain barrier abnormality.

Lorenzi¹,

Karam²,

McIlroy³

et al. 1980

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Increased growth hormone response to dopamine infusion in insulin-dependent diabetic subjects: indication of possible blood-brain barrier abnormality.

Lorenzi¹,

Karam²,

McIlroy³

et al. 1980

J. Clin. Invest.

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“…The rise in GH produced by amphetamine does not differ between the (+) and (-) isomers (Langer & Matussek, 1977) and this, together with the fact that the effect is not blocked by pimozide suggests that this response is noradrenergic (Sachar, Gruen, Altman, Halpern & Frantz, 1976). Dopamine infusion has been reported to increase the secretion of GH in some studies (Burrow, May, Spaulding & Donabedian, 1977, Leebaw et al, 1978 Increases synthesis of dopamine and noradrenaline and 5-HT 'Indirect presynaptic agent-releases biogenic amines,-noradrenaline and dopamine and blocks re-uptake-increase in turnover of dopamine, noradrenaline and ? 5-HT.…”

Section: Anxiolyticsmentioning

confidence: 87%

Neuroendocrine markers of CNS drug effects.

Johnstone¹,

Ferrier²

1980

Brit J Clinical Pharma

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“…infusion of DA, which does not cross the blood brain barrier, induces GH increase in normal subjects (Burrow et al 1977;Langer et al 1978;Woolf et al 1979), while DA administration to in vitro pituitaries from both normal and acromegalic subjects reversely causes Gil decreases (Goodyer et al 1978;Peillon et al 1979). These findings suggest a direct action of DA on pituitary somatotropes in man, although such contradictory responses to DA are still open to discussion.…”

Section: Discussionmentioning

confidence: 99%

Evidence for endogenous dopaminergic control of GH release in man.

Hanew

Sasaki

Yoshinaga

1981

Tohoku J. Exp. Med.

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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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TRH and Dopamine Interactions Affecting Pituitary Hormone Secretion

Cited by 154 publications

References 26 publications

Increased growth hormone response to dopamine infusion in insulin-dependent diabetic subjects: indication of possible blood-brain barrier abnormality.

Increased growth hormone response to dopamine infusion in insulin-dependent diabetic subjects: indication of possible blood-brain barrier abnormality.

Neuroendocrine markers of CNS drug effects.

Evidence for endogenous dopaminergic control of GH release in man.

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