Neurotransmitters--control of growth hormone (GH) and prolactin (PRL) secretion: the adrenergic and serotoninergic modulation of GH and PRL in man.
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Biomedical subjects
Publications and source records attributed to E Del Pozo.
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The effect of a new soluble ester of 1-5 hydroxytryptophan (1-5 HTP, Ro 3-5940, 200 mg infusion) on prolactin (PRL) and growth hormone (GH) release was tested in 11 young, healthy subjects (6 men, 5 women). To minimize side-effects, peripheral decarboxylase inhibition was achieved with benserazide (Ro 4-4602.) PRL increased significantly (P less than 0.01) after benserazide alone in all subjects. A further significant increase (P less than 0.01) of PRL plasma levels occurred only in women up to 90 min after the infusion of 1-5 HTP was discontinued. Benserazide administration had no effect of basal GH levels, but a significant increase of GH release (P less than 0.01) was noticed 30-120 min after the end of 1-5 HTP infusion in both men and women. The mean peak value of GH plasma levels after 1-5 HTP administration was 32.0 +/- 8.8 ng/ml. It was postulated that benserazide penetrated at the level of the pituitary, decreasing the synthesis of dopamine and consequently reducing its known inhibitory effect on PRL release. The PRL increase (statistically significant only in women), as well as the release of GH after 1-5 HTP infusion, was considered as further evidence for stimulatory serotoninergic control of both PRL and GH secretion.
Five volunteers with normal ovarian cycles received oral doses of 2 X 2.5 mg or 3 X 2.5 mg bromocriptin (CB 154)/day respectively. The treatment started at the onset of menstruation and lasted on complete cycle. In addition to the decrease of prolactin secretion, a reduction of plasma progesterone concentrations during the corpus luteum phase was demonstrated. This fall of progesterone seemed to be preferentially due to bromocriptin-induced hypoprolactinaemia and not to direct ovarian effects of the drug.
Mastodynia has previously been treated with gestagens or gestagen-based ovulation inhibitors with only marginal success. No other satisfactory therapy was available and in the search for a better treatment, the effectiveness of long term administration of the prolactin inhibitor bromocryptine (CB 154) to 15 patients was evaluated. Five of the subjects exhibited mammary secretion as well as mastodynia which, accorind to palpatorial, cytological and X-ray criteria, was not caused by intraductal pathology. After two to four weeks treatment with 5 mg CB 154 per day ten patients recovered fully, three showed some improvement and two were totally resistant to the treatment. Plasma prolactin levels during the follicular stage measured prior to treatment were in the normal range. All the patients continued to ovulate during the course of treatment despite the irrefutable fact that prolactin release from the pituitary was inhibited. Since there was a similar inhibition of prolactin secretion in the two patients who were resistant to treatment, it would seem that prolactin though probably very important, cannot be the only decisive factor in the hormonal control of mystodynia. Further observations showed that the premenstrual syndrome can also be successfully treated with CB 154. Upon withdrawal of treatment the possibility or relapse must be considered.
There is little information about the action of ergot derivatives other than bromocriptine (CB 154) on plasma prolactin and milk secretion in human beings. In a recent report it has been suggested that ergonovine might interfere with lactation when administered post partum. The present study shows that methyl-ergonovine (Methergine), a closely related compound, has no action on prolactin or milk secretion as measured in a group of 10 breast feeding mothers in comparison with another 10 untreated puerperas.
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