Pituitary Gland

Pituitary Gland

The pituitary gland, also known as the hypophy-sis (FIGURE 16-6), is located at the base of the brain,attached to the hypothalamus, superiorly, by a stalk called the infundibulum. The pituitary is about 1 cm in diameter. It lies in the sella turcica of the sphenoid bone and secretes a number of different hormones. The description of the pituitary gland’s appearance is that of a “pea on a stalk.” Arterial blood is delivered to the pituitary gland via hypophyseal branches of the internal carotid arteries. Veins leaving the gland drain into the dural sinuses.

The anterior pituitary and posterior pituitary lobes have differing functions. The anterior pituitary gland is also called the adenohypophysis and is composed of glandular tissue. It manufactures and releases a variety of hormones. The anterior lobe has three regions:

■■Pars distalis: The largest, most anterior part of thepituitary gland.

■■Pars tuberalis: The extension that wraps aroundthe adjacent area of the infundibulum.

■■Pars intermedia: The slender and narrow band that borders the posterior lobe of the pituitary gland; this section may secrete two types ofmelanocytestimulating hormone, also known as melanotropin. It stimulates the melanocytes ofthe skin to increase production of melanin, and the release of melanocyte-stimulating hormone isinhibited by dopamine.

Releasing hormones from the hypothalamus control the anterior pituitary’s secretion and travelin the hypothalamus’s capillary network. These fenestrated capillaries contain structures that resem-ble pores and form the hypophyseal portal veins passing along the pituitary stalk to the capillary network of the anterior pituitary (FIGURE 16-7). The hypothalamus releases substances that are car-ried directly to the anterior pituitary via the blood. Releasing actions of the anterior pituitary are mostly stimulatory, although some have inhibitory effects. The primary and secondary capillary plexuses, along with the hypophyseal portal veins, are the structures that comprise the hypophyseal portal system. Via this system, releasing and inhibiting hormones from the ventral hypothalamus circulate to the anterior­ pituitary and regulate its hormone secre-tion. ­Releasing hormones stimulate synthesis and secretion of one or several hormones at the anterior lobe, while inhibiting hormones prevent this from occurring.

Anterior Pituitary Hormones

The anterior pituitary consists of dense, collagenous connective tissue (FIGURE 16-6), and is known as the “master endocrine gland.” Its numerous hor-mones, which are all proteins, regulate the activity of other endocrine glands. It has six types of secre-tory cells: growth hormone (GH), prolactin­ (PRL), thyroid­-stimulating hormone (TSH), ACTH, follicle­-stimulating hormone (FSH), and ­luteinizing hormone (LH).

An appropriate chemical stimulus from the hypo-thalamus causes the anterior pituitary to release one or more of its hormones. Each target cell is able to distin-guish its received messages and respond so it secretes the correct hormone, regulated by the specific releas-ing hormones. Hormone release is likewise shut off,according to specific inhibiting hormones. The tropichormones, also called tropins, regulate the secretoryactions of other endocrine glands. These include TSH, ACTH, FSH, and LH. Except for GH, all the anterior pituitary hormones affect their target cells via a cAMP second messenger system.

Growth Hormone

GH is produced by somatotropic cells of the anterior pituitary and is also called somatotropin. It stimu-lates cells to grow and divide more frequently and enhances the movement of amino acids to stimulate growth. This hormone has both direct metabolic and growth-promoting actions. It mobilizes fats for transport to cells, which increase blood ­levels of fatty acids to be used for fuel. GH decreases rates of glucose­ uptake and metabolism to conserve glu-cose. It encourages liver breakdown of glycogen so glucose can be released to the blood. Therefore, GH is said to have glucose-sparing actions and anti-­insulin effects. It also increases amino acid uptakeinto the cells so these acids can be incorporated into proteins. The hypothalamus, as well as the patient’s nutritional state, influences GH secretion via GH-­ releasing hormone and GH release-inhibiting hor-mone. More GH is released when protein is deficient and blood glucose is low. Also, ghrelin, known as the “hunger­ hormone,” stimulates the release of GH.

GH secretion­ undergoes a diurnal cycle (FIGURE­16-8), in that during sleep and strenuous exercise, blood levels­ of GH are at their highest. As we age, GH secretion declines gradually.

GH uses various growth-promoting proteins known as insulin-like growth factors (IGFs), which allow it to have indirect growth-enhancing effects. IGFs are produced by tissues such as the liver, bone, and skeletal muscle in response to GH. In the liver, IGFs act as hormones, but those produced by other tissues act locally as paracrines. The actions required for growth as stimulated by IGFs are:

■■Uptake of blood nutrients for incorporation into proteins and DNA, which allows growth by cellvision.

■■Collagen formation and bone matrix deposition.The major targets of GH are bone and skeletal muscle. Long bone growth occurs via epiphyseal stimulation. Muscle mass increases by stimulation of skeletal muscles.

Prolactin

PRL is a protein hormone that controls milk produc-tion in women after they give birth. In males, it may also help to maintain sperm production. Prolactin is also called mammotropin. Elevated levels of PRL can interrupt sexual function in both females and males. The secretion of PRL is regulated by a neuroendocrinereflex, a reflex involving both the endocrine and ner-vous systems (FIGURE 16-9). During the breastfeeding process, sensory fibers in the breast are stimulated, sending nerve impulses to the hypothalamus. The hypothalamus responds by secreting PRL-releasing hormone, causing PRL release. The PRL-­inhibiting hormone is dopamine. Lower PRL-inhibiting hor-mone secretion causes increased PRL release. There are many PRL-releasing factors, one of which is ­thyroid-releasing hormone. In women, estrogen stim-ulates PRL release, which is part of the cause of breast tenderness before menstruation.

Thyroid-Stimulating Hormone

TSH controls the thyroid and TSH secretion is reg-ulated by the hypothalamus via thyroid-releasinghormone. Receptors in the hypothalamus controllevels of circulating thyroxine. When these levels are low, receptors signal the hypothalamus to release TSH releasing hormone. As thyroxine levels increase, TSH releasing hormone secretion declines (FIGURE 16-10) in a process called negative feedback control of TSH secretion. The secretion of TSH releasing hormone is also stimulated by cold and stress. TSH is also known as thyrotropin.

Adrenocorticotropic Hormone

ACTH controls hormone secretion from the cortex of the adrenal gland, partly via corticotropin-releasinghormone (CRH) from the hypothalamus. Stress mayalso increase ACTH secretion. Negative feedback con-trols the secretion of ACTH (FIGURE 16 -11). ACTH is also known as corticotropin, because it is secreted by the corticotropic cells. It stimulates the release of corticosteroid hormones from the adrenal cortex, of which glucocorticoids are most important because they play a role in resisting stressors. Every day, the release of ACTH occurs in a rhythm, wherein levels are highest in the morning just before we wake up. As levels of glucocorticoids rise, CRH secretion is blocked, as is ACTH release. However, normal ACTH rhythm can be altered by factors such as fever, all types of stressors, and hypoglycemia.

Gonadotropins

FSH and LH are gonadotropins affecting the repro-ductive organs or gonads. In males, these are the testes and in females, the ovaries. In the testes, FSHstimulates the production of sperm, and in the ova-ries, it stimulates the production of eggs. In males, LH stimulates the interstitial cells in the testes to produce testosterone, and in females, LH along with FSH causes the ovarian follicle to mature. LH then triggers ovulation and regulates ovarian hormone synthesis and release. Gonadotropins become more active during puberty, prompted by hypothalamic release of gonadotropin-releasing hormone (GRH). The hormone called inhibin decreases FSH levels in both males and females.

Posterior Pituitary and Hypothalamic Hormones

The posterior pituitary differs from the anterior pituitary, in that it is made up of mostly nerve fibers and neuroglial cells called pituicytes (­FIGURE 16-12). The hypothalamic neurons are located in supra-optic or paraventricular nuclei, synthesizing oxy-tocin and antidiuretic hormone (ADH). These neurohormones­ are received from the hypothalamus.The posterior pituitary actually functions as a storage area for hormones instead of a manufacturing area. Together, the infundibulum and the posterior lobe of the pituitary gland make up the neurohypophysis­. This term is often used to describe just the posterior lobe itself, but this is incorrect. The posterior lobe is actually part of the brain and is formed by a down growth of ­hypothalamic tissue. Its neural connection with the hypothalamus is via a nerve bundle called the hypothalamic­-hypophyseal tract, which runs through the infundibulum. Therefore, if there is a transection of the infundibulum, oxytocin and ADH would be lost. The hypothalamic-hypophyseal tract is formed by neurons in the supraoptic and paraventric-ular nuclei of the hypothalamus.

Specialized supraoptic and paraventricular neu-rons of the hypothalamus produce the posterior pitu-itary’s hormones, ADH and oxytocin, respectively. ADH is also called vasopressin. Nerve impulses from the hypothalamus release these hormones into the blood. A diuretic is a chemical that increases urine production, whereas an antidiuretic decreases urine formation (FIGURE 16-13).

Antidiuretic Hormone

ADH regulates the water concentration of body flu-ids by reducing water excretion by the kidneys. It acts to prevent both water overload and dehydration from occurring. Decreased levels of ADH cause polyuria and diabetes insipidus.

Osmoreceptors sense increases in osmotic pres-sure due to dehydration and use ADH to signal the kidneys to produce less urine. If too much water is in the body, ADH release is inhibited and urine produc-tion increases. ADH targets kidney tubules via cAMP, and the tubules then reabsorb more water from the forming urine returning it to the bloodstream. There-fore, less urine is produced and solute concentrations of the blood decline. This triggers the osmoreceptors to stop depolarizing, which nearly stops the release of ADH. Other triggers for ADH release include low blood pressure, pain, morphine, barbiturates, and nicotine. Alcohol intake inhibits ADH secretion and increases urine output, as does consuming high amounts of water. An alcoholic hangover is signi-fied by dehydration, including intense thirst and dry mouth. Oppositely, diuretics antagonize ADH effects, removing water from the body. They are used for cer-tain types of hypertension and edema such as in con-gestive heart failure. In severe blood loss conditions, extremely high amounts of ADH are released, causing vasoconstriction mostly of visceral blood vessels. The blood pressure then rises. This response uses different ADH receptors on vascular smooth muscle; hence, the alternate name of ADH is vasopressin.

Oxytocin

Oxytocin stimulates uterine contractions during childbirth and milk letdown, which is the ejection of milk from the breast glands soon after suckling begins.

Oxytocin receptors peak in number near the end of pregnancy and the hormone’s stimulatory effects are most effective on uterine smooth muscle. Oxytocin release, at this time, is triggered by afferent impulses that reach the hypothalamus. When blood levels of oxytocin rise, uterine contractions increase until expulsion of the fetus occurs. In the brain, oxytocin acts as a neurotransmitter and is involved in affection and sexual behaviors as well as promoting trust, nur-turing behaviors, and the bonding of two individuals as a “couple.” TABLE 16-3 discusses the pituitary gland hormones in greater detail.

1. Define the term gonadotropin.

2. List the effects of ACTH and PRL.

3. List the hormones stored in the posterior lobe of the pituitary gland.

4. Describe the physiology of vasopressin and oxytocin.