The Endocrine System / The Pituitary Gland - Advanced Version

What is it?

Anatomy

The pituitary gland is a small oval endocrine gland that lies at the base of the brain, nestled in a bony structure called the sella turcica. It is sometimes called the master gland of the body because all the other endocrine glands depend on its secretions for stimulation.

Functionally speaking, the pituitary is divided into two distinct lobes that arise from different embryological sources:

• The anterior (front) lobe, or adenohypophysis, grows upward from the pharyngeal tissue at the roof of the mouth.
• The posterior (back) lobe, or neurohypophysis, grows downward from neural tissue. It is structurally continuous with the hypothalamus of the brain, to which it remains attached by the hypophyseal, or pituitary, stalk.

The two sections of the pituitary gland produce a number of different hormones which act on different target glands or cells.

The hypothalamus controls almost all secretions of the pituitary. The posterior lobe is controlled by nerve fibers that originate in hypothalamic neurons and the anterior lobe by substances that are transported from the hypothalamus by tiny blood vessels (see image below).

This diagram shows the relationship of the pituitary gland and the hypothalamus and the flow of hormone production.

Hormones Produced by the Anterior Pituitary

Hormones are chemicals which circulate in the blood stream and spread around the body to carry messages or signals to different parts of the body. The name hormone comes from the Greek word hormao meaning "I excite" and refers to the fact that each hormone excites or stimulates a particular part of the body known as the target gland.

Hormones are made in endocrine glands and passed from the cells of the gland directly into the blood flowing through the gland. Generally, the higher the amount of hormone that is in the blood, the greater the effect its the targets.

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Table of pituitary hormones, targets and function

Control of hormone production is monitored continuously and regulated using feedback loops.

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Table of Hormones Under the Control of the Pituitary Gland

Anterior Pituitary Hormones

• Adrenocorticotrophic Hormone (ACTH)
• Thyroid-Stimulating Hormone (TSH) or thyrotropin
• Luteinising Hormone (LH)
• Follicle-Stimulating Hormone (FSH)
• Prolactin (PRL)
• Growth Hormone (GH)
• Melanocyte-Stimulating Hormone (MSH)

Hormones Produced by the Hypothalamus

The secretion of hormones from the anterior pituitary is controlled by the production of hormones by the hypothalamus. Although there are a number of different hormones they can be split into two main types:

• hormones that tell the pituitary to switch on production of a hormone (a releasing hormone); and
• hormones that tell the pituitary to switch off production of a hormone (an inhibiting hormone).

Thyrotropin

Thyrotropin is also called thyroid-stimulating hormone (TSH). Thyrotropin-producing cells (thyrotrophs) make up about 10 percent of the anterior pituitary and are located mainly in the center of the gland. Thyrotropin becomes attached firmly to receptors on the surface of the thyroid cells, forming thyroid follicles in the thyroid gland. Following binding, a complex train of events occurs so that preformed thyroid hormones are secreted and steps are set in motion for the synthesis of additional thyroid hormones. Thyrotropin exerts other pervasive effects. It stimulates the growth of thyroid cells and leads to increased blood flow through the gland. It also enhances the breakdown of thyroglobulin, a large thyroid-hormone-containing glycoprotein that is stored within the follicles of the thyroid gland.

The levels of thyrotropin in circulating fluids become elevated during thyroid hormone deficiency because there is no negative feedback inhibition of pituitary thyrotropin release by thyroid hormone. Elevated thyrotropin levels are found in other pathological states, including the presence of a thyrotropin-producing pituitary tumor. Low serum thyrotropin levels occur following damage to cells in the hypothalamus that produce thyrotropin-releasing hormone (TRH), following damage to the pituitary stalk, or, finally, following damage to the thyrotrophs themselves. Tests of increased sensitivity have made the measurement of thyrotropin in blood valuable in detecting subtle changes of both thyroid hyperfunction and hypofunction.

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Gonadotropins

Gonadotrophs, which amount to about 7 percent of all pituitary cells, secrete two hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), but not in equal amount. The rate of secretion varies widely at different ages and at different times in the menstrual cycle of the female. Secretion of LH and FSH is low before puberty in both sexes. After puberty, about five times more LH than FSH is secreted. During menstrual cycles there is a dramatic rise in both hormones at the time of ovulation (see the ovary), and secretion increases as much as 15-fold following {menopause} menopause.

In men FSH stimulates the development of spermatozoa, in large part by acting on special cells in the testes called Sertoli cells. In women FSH stimulates the synthesis of estrogens as well as the maturation of cells lining the spherical, egg-containing structures known as the Graafian follicles. In menstruating women, there is a preovulatory surge in FSH levels in the blood. Inhibin, a hormone secreted by the Graafian follicles of the ovary and the Sertoli cells of the testis, inhibits the secretion of FSH from the pituitary gonadotroph.

In men androgens (male hormones) are secreted by specialized cells called Leydig cells, a process stimulated by LH. In women a preovulatory surge of LH is essential for rupture of the Graafian follicle so that the egg can be discharged on its journey to the uterus. The empty follicle becomes filled with other, progesterone-producing cells, transforming it into a corpus luteum.

When a disease process leads to encroachment on the cells of the pituitary gland, usually the first evidence of cell failure is in the gonadotroph. Thus, disappearance of menstrual periods may be the first sign of a pituitary tumor in the female. In the male the most common symptom of gonadotropin deficiency is impotence. Isolated deficiencies of both LH and FSH do occur, but only rarely. In a male, LH deficiency alone leads to the appearance of what has been described as a “fertile eunuch”; there is sufficient FSH present to permit the maturation of spermatozoa, but because of the LH deficiency the man has, nonetheless, many of the characteristics of a castrate. Tumors also can produce an excess of LH or FSH, and pituitary tumors that secrete only the nonspecific, hormonally inactive alpha unit of glycoprotein hormones are not rare.

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Corticotropin or ACTH

Corticotropin, also called adrenocorticotropin hormone (ACTH), is a segment of a much larger prohormone glycoprotein molecule called pro-opiomelanocortin, which is synthesized by pituitary corticotrophs. This prohormone is split into a number of biologically active polypeptide fragments when the secretory granule is discharged from the cell. Among these hormones are corticotropin, whose major action is to stimulate growth and secretion of the cells of the adrenal cortex; alpha- and beta-melanotropin (melanocyte-stimulating hormone, MSH), which increases pigmentation of the skin; beta-lipotropin (LPH), which stimulates the release of fatty acids from adipose tissue; a small fragment of ACTH thought to improve memory; and beta-endorphin, a polypeptide that has excited a good deal of popular as well as scientific interest (see the adrenal cortex).

Beta-endorphins (along with the enkephalins, which are neuromodulators) were discovered when investigators postulated that, since opiates such as morphine bind firmly to cell-surface receptors, there must exist natural substances that do likewise and have a narcotic action. The endorphins and enkephalins are known, therefore, as endogenous (self-generated) opiates or opioids. They have powerful painkilling properties. Beta-endorphins instilled in the spinal fluid are capable of alleviating otherwise intractable pain in cancer patients. It has often been observed that severely traumatized individuals, those in battle, for example, appear to be free of pain. This phenomenon is due to the simultaneous release of beta-endorphin along with corticotropin in response to the stressful stimulus of the injury. There have also been reports of children with endorphin-producing pituitary tumors who are highly insensitive to pain. In addition, the release of endorphin or enkephalin may account for the euphoria (“high”) experienced by long-distance runners. Finally, there is evidence, not fully accepted, that endogenous opioids stimulate appetite. This is seen in rats and obese persons who have a rare disease called Prader-Labhart-Willi syndrome. In these instances, the appetite is diminished after the administration of a narcotic antagonist, such as naloxone.

Hyperplasia or adenoma of corticotrophs gives rise to the constellation of symptoms called Cushing's syndrome (discussed in more detail on the next page). A deficiency of corticotropin also occurs both as part of the multiple deficiencies of panhypopituitarism and as an isolated defect. The diagnosis of corticotropin deficiency is important because afflicted persons who are also subjected to stress can succumb to severe shock. Once frequently administered in the treatment of disorders including allergic states, collagen disorders, and autoimmune diseases, corticotropin has been largely displaced by a number of synthetic variants of adrenal steroids.

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Melanocyte-Stimulating Hormone (MSH)

Melanocyte-stimulating hormone gets its name because of its effect on melanocytes: skin cells that contain the black pigment, melanin. In humans, melanocytes are responsible for moles, freckles, and suntan (and, if they turn cancerous, melanoma).

In most vertebrates, MSH is produced by an intermediate lobe of the pituitary gland. Its secretion causes a dramatic darkening of the skin of fishes, amphibians, and reptiles. The darkening occurs as granules of melanin spread through the branches of specialized melanocytes called melanophores.

Prolactin

Prolactin is a hormone produced by the anterior pituitary gland in both men and women. It is known as a gonadotrophic hormone as it affects the gonads (testes and ovaries). It also has an effect on other organs in the body, however, only the effects on the reproductive organs will be discussed here.

In males, prolactin influences the production of testosterone and affects sperm production. In conditions where prolactin secretion is increased (hyperprolactinaemia), testosterone levels drop and sperm production is reduced or absent, resulting in male infertility.

On the evolutionary scale, prolactin is an ancient hormone serving multiple roles in mediating the care of progeny (it has been called the “parenting” hormone). Prolactin is a large protein molecule synthesized and secreted from cells, the lactotrophs, which compose 20 percent of the anterior pituitary gland and are located largely in the two lateral portions. Unlike other anterior pituitary cells whose activities are stimulated by hypothalamic-releasing hormones, the major modulating influence on lactotroph secretion is the inhibitory effect of the neurotransmitter dopamine, which, in the case of prolactin, functions as a hypothalamic neurohormone.

The main action of prolactin in females is the induction and maintenance of lactation (breastfeeding). Prolactin levels build up during pregnancy but milk secretion does not begin until after birth. As an infant suckles, prolactin is released into the mother's blood stream, causing the milk glands to produce more milk. Prolactin and other hormones are responsible for the development of mammary glands during pregnancy. Prolactin also affects the ovaries. The main target area is the corpus luteum, the secretory organ formed from the ruptured ovarian follicle after ovulation. High prolactin levels lead to reduced progesterone function. The result of hyperprolactinaemia can be the non-appearance of menarche (beginning of menstruation at puberty), amenorrhoea (absence of menstruation in a woman after puberty) and anovulatory menstrual cycles (absence of ovulation i.e. no mature eggs produced). These effects can be the basis of female infertility.

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Growth Hormone

Somatotrophs are plentiful in the pituitary, constituting 40 percent of the gland. They are located predominantly in the lateral lobes and secrete between one and two milligrams of growth hormone (GH; also called somatotropin) per day. Growth hormone stimulates growth, not only of bone but of essentially all the tissues of the body. In biochemical terms, growth hormone simultaneously stimulates protein synthesis in tissues and enhances the breakdown of fat to provide the energy for the stimulated growth. Growth hormone is also an insulin antagonist and, in susceptible individuals, can lead to elevated sugar levels in the blood and diabetes mellitus.

While GH may act on tissues directly, much of its effect is mediated by way of stimulating the liver and other tissues to manufacture and release secondary hormones, called somatomedins, which partly mimic the action of insulin. During childhood, somatomedin levels in the serum rise progressively with age, with an accelerated increase occurring at the time of the growth spurt of puberty, followed by a reduction to adult levels.

Growth hormone secretion is stimulated by growth hormone-releasing hormone (GHRH; also known as somatocrinin) and is inhibited by somatostatin. There are prominent daily fluctuations in growth hormone secretion in normal individuals, with the largest increase occurring shortly after the onset of sleep. Again, this increase is most pronounced at the time of puberty. Growth hormone levels in the serum are elevated in individuals with tumors that produce growth hormone, and its levels are unresponsive to stimulation in states of malnutrition.

The term acromegaly refers to the enlargement of the distal parts of the body; there is, in fact, progressive enlargement of the hands, feet, chin, and nose. Most other organs also become enlarged. The presence of a pituitary tumor causes severe headaches, and the pressure of the tumor on the optic chiasm causes visual defects.

The acromegalic patient has overgrown supraorbital ridges, enlarged nasal sinuses that give a sonorous quality to the voice, an overgrown jaw, spaces between the teeth, and an enlarged tongue. The skin thickens, producing a permanently furrowed brow. The enlarged fingers are no longer tapered and become spatulated.

Because the metabolic actions of growth hormone are antagonistic to those of insulin, some acromegalic patients develop diabetes mellitus and are subject to all of its complications. Other problems include elevated blood pressure, heart disease, and progressive arthritis. Finally, because some of these tumors produce prolactin as well as growth hormone, males may have enlarged breasts, and both sexes may show abnormal lactation (milk secretion). Acromegaly can be treated with a considerable degree of success with surgery, with X-ray therapy, and with drugs such as bromocriptine or a synthetic, long-acting somatostatin.

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