Prolactin secretion is under tonic inhibitory control by the hypothalamic secretion of dopamine (40). Therefore, disease states characterized by decreased dopamine secretion or any condition that interrupts transport of dopamine down the infundibular stalk to the pituitary gland will result in increased synthesis of prolactin. In this respect, prolactin is unique in comparison with all other pituitary hormones: It is predominantly under tonic inhibition, and release of control produces an increase in secretion. Clinically, increased prolactin levels are associated with amenorrhea and galactorrhea, and hyperprolactinemia should be suspected in any individual with symptoms of either of these conditions.
Although prolactin appears to be primarily under inhibitory control, many stimuli can elicit its release, including breast manipulation, drugs, stress, exercise, and certain foods.
Hormones that may stimulate prolactin release include TRH, vasopressin, γ -aminobutyric acid (GABA), dopamine, β-endorphin, vasoactive intestinal peptide (VIP), epidermal growth factor, angiotensin II, and possibly GnRH (41–43). The relative contributions of these substances under normal conditions remain to be determined.
Thyroid-Stimulating Hormone, Adrenocorticotropic Hormone, and Growth Hormone
The other hormones produced by the anterior pituitary are TSH, ACTH, and GH. Thyroid-stimulating hormone is secreted by the pituitary thyrotrophs in response to TRH. As with GnRH, TRH is synthesized primarily in the arcuate nucleus of the hypothalamus and is secreted into the portal circulation for transport to the pituitary. In addition to stimulating TSH release, TRH is a major stimulus for the release of prolactin. Thyroid-stimulating hormone stimulates release of T3 and T4 from the thyroid gland, which in turn has a negative feedback effect on pituitary TSH secretion. Abnormalities of thyroid secretion (both hyper-and hypothyroidism) are frequently associated with ovulatory dysfunction as a result of diverse actions on the hypothalamic–pituitary–ovarian axis (44).
Adrenocorticotrophic hormone is secreted by the anterior pituitary in response to another hypothalamic-releasing factor, CRH, and stimulates the release of adrenal glucocorticoids.
Unlike the other anterior pituitary products, ACTH secretion has a diurnal variation with an early morning peak and a late evening nadir. As with the other pituitary hormones, ACTH secretion is negatively regulated by feedback from its primary end product, which in this case is cortisol.
The anterior pituitary hormone that is secreted in the greatest absolute amount is GH. It is secreted in response to the hypothalamic-releasing factor, GHRH, and by thyroid hormone and glucocorticoids. This hormone is secreted in a pulsatile fashion but with peak release occurring during sleep. In addition to its vital role in the stimulation of linear growth, GH plays a diverse role in physiologic hemostasis. The hormone plays a role in bone mitogenesis, CNS function (improved memory, cognition, and mood), body composition, breast development, and cardiovascular function. It also affects insulin regulation and acts anabolically. Growth hormone appears to have a role in the regulation of ovarian function, although the degree to which it serves this role in normal physiology is unclear (45).