Control of prolactin secretion
- 1 December 1990
- journal article
- review article
- Published by Springer Nature in Journal of Molecular Medicine
- Vol. 68 (23) , 1157-1167
- https://doi.org/10.1007/bf01815271
Abstract
Prolactin is a 21,500 Dalton single-chain polypeptide hormone but may occur in 50 kDa and 150 kDa molecular variants. These large PRL variants may be secreted predominantly; this condition is termed “macroprolactinemia”. It is characterized by high immunological and normal biological serum levels of prolactin, and lack of clinical symptoms of hyperprolactinemia. The information on PRL is encoded on chromosome 6. Transcription can be enhanced and suppressed by a variety of hormonal factors. PRL is secreted in a pulsatile fashion; it displays a circadian rhythm (with a maximum during sleep) and is stimulated by some amino acids. PRL also responds to mechanical stimulation of the breast. PRL rises during pregnancy, and maintainance of hyperprolactinemia (and, thereby, physiological infertility) is dependent on the frequency and duration of breast feedings. Hypothalamic regulation of prolactin mainly involves tonic inhibition via portal dopamine. The physiological importance of various stimulating factors present in the hypothalamus is still incompletely understood. In particular, there is still no place for TRH in PRL physiology. PRL is released in response to stress; this response may be mediated by opioids. The low-estrogen, low-gonadotropin amenorrhea of endurancetraining women is not mediated by prolactin, however. Estrogens stimulate PRL gene transcription via at least two independent mechanisms. There are many clinical examples of this estrogen effect on prolactin serum levels, and also on the growth of prolactinomas. Mild hyperprolactinemia remains an enigma which cannot satisfactorily be resolved by biochemical or radiological testing. The border between “normal” and “elevated” prolactin is illdefined. The possibility of macroprolactinemia complicates this matter even further. The number of drugs which suppress prolactin by acting on pituitary D2 receptors, and which are useful in the treatment of hyperprolactinemia, continues to increase. In the field of ergot alkaloids, parenteral application appears to be a logical solution to the problem of the high first-pass effect; in addition, this form of treatment is frequently better tolerated than the oral route. Prolactinoma development is presently being studied employing molecular biological techniques; the question of whether tumorigenesis can be attributed to specific defects of gene regulation remains to be answered.Keywords
This publication has 132 references indexed in Scilit:
- Autoradiographic Identification of Prolactin Binding Sites in Rat Median EminenceNeuroendocrinology, 1989
- Three growth hormone- and two prolactin-related novel peptides of Mr 13,000–18,000 identified in the anterior pituitaryBiochemical and Biophysical Research Communications, 1988
- Occurrence of prolactinoma after estrogen treatment in a girl with constitutional tall statureThe Journal of Pediatrics, 1988
- Combined thyrotroph and lactotroph cell hyperplasia simulating prolactin-secreting pituitary adenoma in long-standing primary hypothyroidismSurgical Neurology, 1988
- Endocrine aspects of lactation and postpartum infertilityJournal of Steroid Biochemistry, 1987
- Catecholamines and Pituitary Function. VI. Effect of Different Dopamine Doses on TRH-Induced Prolactin Release in Women with Pathological HyperprolactinemiaHormone and Metabolic Research, 1987
- Dopaminergic Inhibition of Prolactin Release and Calcium Influx Induced by Neurotensin in Anterior Pituitary Is Independent of Cyclic AMP SystemJournal of Neurochemistry, 1986
- Evidence for Increased Endogenous Dopaminergic Inhibition of Aldosterone Secretion in ProlactinomaHormone and Metabolic Research, 1986
- Temperature-Induced Hyperprolactinemia during ExerciseHormone and Metabolic Research, 1986
- ALTERED DOPAMINERGIC REGULATION OF THYROTROPHIN RELEASE IN PATIENTS WITH PROLACTINOMAS: COMPARISON WITH OTHER TESTS OF HYPOTHALAMIC-PITUITARY FUNCTIONClinical Endocrinology, 1981