The pituitary gland is a pea sized region of specialized endocrine cells and neurons located behind the optic chiasm and enclosed in a bony structure called the sella turcica, or Turkish saddle. Although the pituitary is often called the “master gland” of the endocrine system, that label is more appropriate for an adjacent area of brain known as the hypothalamus. As 19th century scientists deciphered the anatomy and physiology of the central nervous system and endocrine glands, the role of the pituitary gradually became clear.
Today, biologists separate pituitary function into the anterior pituitary (adenohypophysis) and posterior pituitary (neurohypophysis). Each will be considered in turn.
The anterior pituitary is connected to the hypothalamus by specialized network of blood vessels known as the hypophyseal portal system. Hypothalamic neurons synthesize proteins called release factors, which signal various populations of pituitary cells to release their hormones directly into the systemic circulation. The major cell types in the anterior pituitary include somatotrophs, lactotrophs, thyrotrophs, gonadotrophs, and corticotrophs.
Somatotrophs produce hGH, or human growth hormone. Growth hormone acts in the liver to stimulate the production of IGF-1 (Insulin-Like Growth Factor-1). IGF-1, in turn, promotes bone and muscle growth prior to puberty. Growth hormone production declines after puberty; its importance in adult physiology remains a matter of debate.
Lactotrophs make a protein hormone called prolactin (Prl). Prolactin stimulates breast development and milk production in females starting in the last trimester of pregnancy. The importance of prolactin in male physiology remains unclear. Males do not lactate under normal circumstances. One exception is a patient with a pituitary tumor called a prolactinoma, whose symptoms include abnormal milk production, also called galactorrhea.
Thyrotrophs produce goiter, which results from an enlarged, swollen thyroid gland.
As a general rule, hypothyroid states (like iodine deficiency) are marked by high TSH levels whereas hyperthyroid states (e.g. Graves disease) are marked by low TSH levels. These phenomena are direct results of feedback inhibition, or loss thereof, by thyroid hormones on the pituitary gland. Excessive levels of T3 and T4 shut off TSH production. Conversely, a lack of thyroid hormone production leads to enhanced TSH release by the pituitary. Similar trends occur with imbalances of other endocrine hormones, most notably cortisol, estrogen, and testosterone.
Gonadotrophs make the hormones FSH (follicle stimulating hormone) and LH (luteinizing hormone). In females, an FSH spike occurs at the beginning of the menstrual cycle. FSH triggers the development of egg follicles and stimulates estrogen production by the ovaries. An LH spike triggers ovulation midway through the menstrual cycle. In males, FSH stimulates sperm production and maturation in the seminiferous tubules of the testes. LH acts in a complementary manner by stimulating testosterone production in specialized testicular cells called Leydig cells.
Corticotrophs produce POMC (pro-opiomelanocortin), a precursor hormone which is cleaved to yield β endorphin, ACTH (adrenocorticotropic hormone), MSH (melanocyte stimulating hormone), and some minor peptides. ACTH triggers the production of the steroid hormone cortisol in the adrenal cortex. Endorphins blunt the transmission of pain signals in the spinal cord. MSH promotes the synthesis of the pigment melanin in the skin, hair, and iris of the eye.
Posterior pituitary
The posterior lobe of the pituitary gland does not make its own hormones. Instead, axons from two groups of hypothalamic neurons – the supraoptic nucleus (SON) and paraventricular nucleus (PVN) – terminate in the posterior pituitary.
These specialized neurons produce the hormones ADH (antidiuretic hormone), also known as vasopressin, and oxytocin. When a person becomes dehydrated, osmoreceptors in the brain trigger ADH release into the systemic circulation. ADH travels to the kidneys where it promotes water reuptake in the epithelial cells lining the collecting ducts.
The exact mechanism of action of ADH remained obscure until 1990, when Peter Agre discovered a class of protein channels, now called aquaporins, which selectively allow water molecules to cross the cell membrane. ADH activates a G-protein coupled receptor on these epithelial cells, triggering an influx of calcium ions, the activation of Protein Kinase C, and the translocation of aquaporins to the cell surface leading to enhanced water reuptake.
Oxytocin has two main functions. First, it triggers uterine contractions when a pregnant woman goes into labor. Second, it promotes the movement of milk from the breast ducts to the nipple by stimulating the contraction of myoepithelial cells lining the ducts. In lactating women, this is sometimes called the milk-let-down reflex. The function of oxytocin in male physiology remains uncertain.
