Regulation of Prolactin and Growth Hormone Secretion

Richards, Gail E.; Holland, F. J.; Aubert, Michel L.; Ganong, William F.; Kaplan, Selna L.; Grumbach, Melvin M.

doi:10.1159/000122989

Cited by 21 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results presented here are compatible with the gener ally accepted concept that E: stimulates prolactin synthesis [4,5,8,10,12,16] and thereby facilitates increased basal PRL secretion [11,18,20,26]. Details of the mechanisms, whereby 2-OH-estrone suppresses PRL secretion [22] are unknown.…”

Section: Discussionsupporting

confidence: 86%

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Wollesen¹,

Knigge²,

Larsen³

1982

Neuroendocrinology

View full text Add to dashboard Cite

This study was undertaken to test whether ratios between plasma concentrations of different estrogens would be more determinant of prolactin (PRL) secretion than plasma concentrations of estrogens per se have been found to be. Oral administration of micronized 17β-estradiol in a dose of 2 mg b.i.d. for 1 month to 7 postmenopausal women raised plasma estrone (E₁) from a median of 29 to 683 pg/ml and plasma 17β-estradiol (E2) from a median of 5.7 to 131 pg/ml. The E₁/E₂ ratios rose from a median of 4.01 to 4.92 (P_Wilcoxon (P_w) > 0.025). Basal serum PRL increased from a median of 79.2 to 100 μlU/ml (P_w) > 0.025). However, the area under the curve of the PRL response to TRH increased from a median of 2,553 mm² before to 3,919 mm² after treatment (P_w <0.025). Highly significant correlations existed between the E1/E2 ratios and the PRL responses to TRHboth before (r_Spearman (r_s) = 0.964) (P_Spearman (P_s) <0.005) and after (r_s = 1.000) (P_s < 0.00025) estradiol treatment, whereas no correlations (P_s <0.679) existed between plasma concentrations of Ei or E2 per se and either basal serum PRL or PRL response to TRH. The regression curves of best fit between the E1/E2 ratios and the PRL responses to TRH were hyperbolic both before (r = 0.884) and after (r = 0.996) treatment. These results, showing that the E1/E2 ratio rather than the plasma Ei or E2 concentrations per se are correlated to the PRL responses to TRH, imply that the metabolic conversion rate of estrogens modulates PRL secretion.

show abstract

Section: Discussionsupporting

confidence: 86%

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Wollesen¹,

Knigge²,

Larsen³

1982

Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…Data obtained in dogs suggested an inhibitory role of serotoninergic pathways on GH secretion, since administration of 5-HT reuptake inhibitors induced a decrease in GH responses to hypoglycaemia, whereas 5-HT receptor antagonist increased the same response [30]. However, a stimulatory role of 5-HT on cGH release has also been suggested, based on the finding that activation of 5-HT neurotransmission with 5-hydroxytryptophan (5-HTP) increases plasma GH levels [31]. Finally, as happened with dogs, based on data obtained in humans, stimulatory, inhibitory or no influence of serotoninergic pathways have been claimed [3, 4, 5, 7, 9, 10, 11].…”

Section: Discussionmentioning

confidence: 99%

Influence of Different Serotonin Receptor Subtypes On Growth Hormone Secretion

Valverde

Peñalva²,

Diéguez

2000

Neuroendocrinology

View full text Add to dashboard Cite

The role of serotonin (5-HT) in the regulation of growth hormone (GH) secretion remains unclear due to the existence of many different receptors that mediate the 5-HT actions, and the lack of suitable specific agonist and antagonist drugs. In the present work we have taken advantage of the recent development of new selective 5-HT drugs in order to clarify the role played by different 5-HT receptor types and subtypes on GH secretion. The experiments were carried out on beagle dogs. GH-releasing hormone (GHRH) increased basal canine GH (cGH) levels from 0.8 ± 0.2 to 8.8 ± 1.7 µg/l at 15 min. Administration of 5-HT_1D receptor agonist sumatriptan (SUM) induced a cGH peak at 30 min of 12.9 ± 2.7 µg/l. The combined administration of GHRH plus SUM strikingly potentiated cGH release with a peak of 36.9 ± 6 µg/l at 30 min (p < 0.05). Pretreatment with the muscarinic receptor antagonist atropine completely abolished the cGH response to SUM, while the cholinergic agonist pyridostigmine (PYR) did not modify this response (15.3 ± 5 µg/l PYR plus SUM vs. SUM alone 12.9 ± 2.7 µg/l). On the other hand, administration of drugs with activity at 5-HT_2A/C receptors showed a stimulatory role for the 5-HT_2C receptor subtype, since LY-53857 (antagonist 5-HT_2A/C) and DOI agonist (5-HT_2A/C) both modified the GH response stimulated by GHRH (AUC 88.5 ± 30.4 and 400 ± 64.6 vs. 267.3 ± 52.6 respectively), while ketanserin (antagonist 5-HT_2A) did not modify this response. The 5-HT₃ antagonist ICS-205–930 failed to modify either basal or GHRH induced GH responses. In conclusion, our data show that 5-HT_1D receptors play a stimulatory role on GH secretion in the dog, possibly by acting through a decrease in hypothalamic somatostatin release. Similarly, the 5-HT_2C receptor subtypes also appear to play a stimulatory role. However, 5-HT_2A and 5-HT₃ receptors do not appear to be involved in the control of basal and GHRH-induced GH secretion.

show abstract

“…In this respect, the fact that both CRT and PRL mean plasma levels were greater in high-IT depressed patients than in low-IT depressed patients, during pre-clonidine pe riods, suggests the stimulating role that the serotonergic system might play in releasing these hypothalamic factors in the former group. In effect, it is a well-known fact that the central serotonergic system is involved in the releasing of corticotrophin-releasing hormone and triggers PRLreleasing mechanisms [3,9,20,22,24,25,31]. Furthermore, the proven fact that fenfluramine (a serotonin depletor agent) [10] is able to induce a quick improvement of high-IT depressed patients [18] provides additional reinforcement to this presumption.…”

Section: Discussionmentioning

confidence: 99%

Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Depressed Patients

et al. 1985

View full text Add to dashboard Cite

Systolic blood pressure (SBP), diastolic blood pressure (DBP), norepinephrine (NE) plasma levels, cortisol (CRT), growth hormone (GH), and prolactin (PRL) plasma levels were investigated in 26 high intestinal tone (high-IT) and 24 low intestinal tone (low-IT) depressed patients, before and after the intramuscular injection of clonidine (2.5 µg/kg). A positive correlation was found between NE, DBP, and Hamilton Depression Rating Scale (HRS) values in low-IT depressed patients, while a negative correlation was found between HRS/IT and NE in high-IT depressed patients. Although clonidine induced significant reduction of SBP in both groups, the drug reduced DBP and NE in the low-IT group, only. CRT mean level was greater in the high-IT than in the low-IT depressed group. However, clonidine was unable to induce changes in CRT, GH, and PRL mean levels in any depressed group. Our results suggest that the clonidine-induced DBP reduction is a reliable index of sympathetic activity in depressed patients and that both parameters (DBP and IT) are useful physiological markers to differentiate two types of depressive syndromes.

show abstract

Regulation of Prolactin and Growth Hormone Secretion

Cited by 21 publications

References 17 publications

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Effect of the Plasma Estrone/17β-Estradiol Ratio on the Prolactin and TSH Responses to TRH

Influence of Different Serotonin Receptor Subtypes On Growth Hormone Secretion

Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Depressed Patients

Contact Info

Product

Resources

About