In the previous chapter we outlined the basic mechanisms of endocrine regulation and its partnership with nervous regulation. We learned how hormones released from endocrine glands into the bloodstream can signal target tissues to alter their functions in ways that promote homeostasis. Our study of neuroendocrine regulation of body function continues in this chapter, in which we explore the structure and function of some of the major endocrine glands. By looking at a few of the important glands and their hormones, a clear picture emerges of how endocrine regulation works. As you learn the specific actions of the major hormones, think of them as part of an overall system of regulating the body’s functions. In later chapters, we will encounter many of these hormones again as we explore the various body functions they regulate.

PITUITARY GLAND

Structure of the Pituitary Gland

The pituitary gland (formerly called the hypophysis) is a small but mighty structure. It measures only 1.2 to 1.5 cm (about ½ inch) across. By weight, it is even less impressive—only about 0.5 gram (¹/₆₀ ounce)! And yet so crucial are the functions of the anterior lobe of the pituitary gland that, in past centuries, it was referred to as the “master gland.”

The pituitary gland has a well-protected location within the skull on the ventral surface of the brain (Figure 19-1). It lies in the pituitary fossa of the sella turcica and is covered by a portion of the dura mater called the pituitary diaphragm. The gland has a stemlike stalk, the infundibulum, which connects it to the hypothalamus of the brain.

FIGURE 19-1 **Location and structure of the pituitary gland.** The pituitary gland is located within the sella turcica of the skull’s sphenoid bone and is connected to the hypothalamus by a stalklike infundibulum. The infundibulum passes through a gap in the portion of the dura mater that covers the pituitary (the pituitary diaphragm). The inset shows that the pituitary is divided into an anterior portion, the adenohypophysis, and a posterior portion, the neurohypophysis. The adenohypophysis is further subdivided into the pars anterior and pars intermedia. The pars intermedia is almost absent in the adult pituitary.

Although the pituitary looks like one gland, it actually consists of two separate glands—the adenohypophysis, or anterior pituitary gland, and the neurohypophysis, or posterior pituitary gland. In the embryo, the adenohypophysis develops from an upward projection of the pharynx and is composed of regular endocrine tissue. The neurohypophysis, on the other hand, develops from a downward projection of the brain and is composed of neurosecretory tissue. These histological differences are incorporated into their names—adeno means “gland,” and neuro means “nervous.” As you may suspect, the hormones secreted by the adenohypophysis serve very different functions from those released by the neurohypophysis.

Adenohypophysis (Anterior Lobe of Pituitary)

The adenohypophysis, the anterior portion of the pituitary gland, is divided into two parts—the pars anterior and the pars intermedia. The pars anterior forms the major portion of the adenohypophysis and is divided from the tiny pars intermedia by a narrow cleft and some connective tissue (see Figure 19-1).

The tissue of the adenohypophysis is composed of irregular clumps of secretory cells supported by fine connective tissue fibers and surrounded by a rich vascular network.

Traditionally, histologists have identified three types of cells according to their affinity for certain types of stains: chromophobes (literally “afraid of color”), acidophils (“acid [stain] lovers”), and basophils (“base [stain] lovers”). All three types are visible in the photomicrograph shown in Figure 19-2. Currently, however, cells of the adenohypophysis are more often classified by their secretions into five types:

1. Somatotrophs—secrete growth hormone (GH)

2. Corticotrophs—secrete adrenocorticotropic hormone (ACTH)

3. Thyrotrophs—secrete thyroid-stimulating hormone (TSH)

4. Lactotrophs—secrete prolactin (PRL)

5. Gonadotrophs—secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH)

Figure 19-3 summarizes the hormones of the adenohypophysis and shows the primary locations of their target cells.

FIGURE 19-3 **Pituitary hormones.** Some of the major hormones of the adenohypophysis and neurohypophysis and their principal target organs.

GROWTH HORMONE

Growth hormone (GH), or somatotropin (STH), promotes bodily growth indirectly by stimulating the liver and other tissues to produce another hormone called insulin-like growth factor 1 (IGF-1), which, in turn, produces most of the effects attributed to GH.

One of the functions of the GH, by way of IGF-1, is to accelerate amino acid transport into cells. Rapid entrance of amino acids from the blood into the cells allows protein anabolism within the cells to accelerate. Increased protein anabolism allows an increased rate of growth. GH promotes the growth of bone, muscle, and other tissues (Box 19-1).

Box 19-1

HEALTH matters

Growth Hormone Abnormalities

Hypersecretion of growth hormone (GH) during the growth years (before ossification of the epiphyseal plates) causes an abnormally rapid rate of skeletal growth. This condition is known as gigantism (see figure, left). Hypersecretion after skeletal fusion has occurred can result in acromegaly, a condition in which cartilage still left in the skeleton continues to form new bone. This abnormal growth may result in a distorted appearance because of the enlargement of the hands, feet, face, jaw (causing separation of the teeth), and other body parts. Overlying soft tissue may also be affected—for instance, the skin often thickens and the pores become more pronounced.

Hyposecretion of GH during growth years may result in stunted body growth, known as pituitary dwarfism (see figure, right). Formerly, patients were treated only with GH extracted from human tissues. Since 1987, the availability of human GH produced by genetically engineered bacteria has made the treatment obtainable for many more patients. However, continuing concerns have been raised about possible adverse side effects associated with human GH from bacterial sources.

In addition to stimulating protein anabolism, GH also stimulates fat metabolism. GH accelerates mobilization of lipids from storage in adipose cells and also speeds up the catabolism of those lipids after they have entered another cell. In this way, GH tends to shift a cell’s use of nutrients away from carbohydrate (glucose) catabolism and toward lipid catabolism as an energy source. Because less glucose is then removed from the blood by cells, the blood glucose levels tend to rise. Thus GH is said to have a hyperglycemic effect. Insulin (from the pancreas) has the opposite effect—it promotes glucose entry into cells, producing a hypoglycemic effect. Therefore GH and insulin function as antagonists. The balance between these two hormones is vital to maintaining a homeostasis of blood glucose levels.

GH affects metabolism in these ways:

Promotes protein anabolism (growth, tissue repair)

Promotes lipid mobilization and catabolism

Indirectly inhibits glucose metabolism

Indirectly increases blood glucose levels

PROLACTIN

Prolactin (PRL), produced by acidophils in the pars anterior, is also called lactogenic hormone. Both names of this hormone suggest its function in “generating” or initiating milk secretion (lactation). During pregnancy, a high level of PRL promotes the development of the breasts in anticipation of milk secretion. At the birth of an infant, PRL in the mother stimulates the mammary glands to begin milk secretion.

Hypersecretion of PRL may cause lactation in nonnursing women, disruption of the menstrual cycle, and impotence in men. Hyposecretion of PRL is usually insignificant except in women who want to nurse their children. Milk production cannot be initiated or maintained without PRL.

TROPIC HORMONES

Tropic hormones are hormones that have a stimulating effect on other endocrine glands. These hormones stimulate the development of their target glands and tend to stimulate synthesis and secretion of the target hormone (Box 19-2). Four principal tropic hormones are produced and secreted by the basophils of the pars anterior:

1. Thyroid-stimulating hormone (TSH), or thyrotropin, promotes and maintains the growth and development of its target gland—the thyroid. TSH also causes the thyroid gland to secrete thyroid hormone.

2. Adrenocorticotropic hormone (ACTH), or adrenocorticotropin, promotes and maintains normal growth and development of the cortex of the adrenal gland. ACTH also stimulates the adrenal cortex to synthesize and secrete some of its hormones.

3. Follicle-stimulating hormone (FSH) stimulates structures within the ovaries, primary follicles, to grow toward maturity. Each follicle contains a developing egg cell (ovum), which is released from the ovary during ovulation. FSH also stimulates the follicle cells to synthesize and secrete estrogens (female sex hormones). In the male, FSH stimulates the development of the seminiferous tubules of the testes and maintains spermatogenesis (sperm production) by them.

4. Luteinizing hormone (LH) stimulates the formation and activity of the corpus luteum of the ovary. The corpus luteum (meaning “yellow body”) is the tissue left behind when a follicle ruptures to release its egg during ovulation. The corpus luteum secretes progesterone and estrogens when stimulated by LH. LH also supports FSH in stimulating the maturation of follicles. In males, LH stimulates interstitial cells in the testes to develop and then synthesize and secrete testosterone (the male sex hormone).

Box 19-2

HEALTH matters

Tropic Hormone Abnormalities

Hypersecretion of the tropic hormones may result from a pituitary tumor. The tropic hormones, produced at higher than normal levels, cause hypersecretion in their target glands. This may result in various effects throughout the body. Early hypersecretion of gonadotropins may lead to an abnormally early onset of puberty.

Hyposecretion of tropic hormones often causes their target glands to secrete less than a normal amount of their hormones. This may disrupt reproduction, kidney function, overall metabolism, and other processes.

FSH and LH are called gonadotropins because they stimulate the growth and maintenance of the gonads (ovaries and testes). During childhood the adenohypophysis secretes insignificant amounts of the gonadotropins. A few years before puberty, gonadotropin secretion is gradually increased. Then, suddenly, their secretion spurts, and the gonads are stimulated to develop and begin their normal functions.

In addition to those listed, the adenohypophysis produces many other hormones in small amounts. Many of these are also produced elsewhere in the body. For example, α-MSH (alpha melanocyte-stimulating hormone) and other melanocortins discussed in Chapter 7 (see p. 179) are produced in the skin and other tissues, with a relatively insignificant amount also produced in the adenohypophysis.

CONTROL OF SECRETION IN THE ADENOHYPOPHYSIS

The cell bodies of neurons in certain parts of the hypothalamus synthesize chemicals that their axons then secrete into the blood. These chemicals, generally called releasing hormones, travel through a complex of small blood vessels called the hypophyseal portal system (Figure 19-4). A portal system is an arrangement of blood vessels in which blood exiting one tissue is immediately carried to a second tissue before being returned to the heart and lungs for oxygenation and redistribution. The hypophyseal portal system carries blood from the hypothalamus directly to the adenohypophysis, where the target cells of the releasing hormones are located. The advantage of a portal system in the hypophysis is that a small amount of hormone can be delivered directly to its target tissue without the great dilution that would occur in the general circulation. The releasing hormones that arrive in the adenohypophysis by means of this portal system influence the secretion of hormones by acidophils and basophils. In this manner, the hypothalamus directly regulates the secretion of the adenohypophysis. You can see that the supposed “master gland” really has a master of its own—the hypothalamus.

FIGURE 19-4 **Hypophyseal portal system.** Neurons in the hypothalamus secrete releasing hormones into veins that carry the releasing hormones directly to the vessels of the adenohypophysis, thus bypassing the normal circulatory route.

The following is a list of some of the important hormones secreted by the hypothalamus into the hypophyseal portal system:

Growth hormone–releasing hormone (GHRH)

Growth hormone–inhibiting hormone (GHIH) (also called somatostatin [SS])

Corticotropin-releasing hormone (CRH)

Thyrotropin-releasing hormone (TRH)

Gonadotropin-releasing hormone (GnRH)

Prolactin-releasing hormone (PRH)

Prolactin-inhibiting hormone (PIH)

Figure 19-5 and Table 19-1 list functions of each releasing hormone. Before consulting the figure or table, try to deduce their functions from their names.

FIGURE 19-5 **Action of hypothalamic hormones.** Hypothalamic hormones have releasing or inhibiting effects on the various cells of the anterior pituitary, thus regulating anterior pituitary secretion—and thus ultimately regulating the effects of anterior pituitary hormones throughout the body. *GnRH,* Gonadotropin-releasing hormone; *GHRH,* growth hormone–releasing hormone; *SS,* somatostatin; *TRH,* thyroid-releasing hormone; *PIH,* prolactin-inhibiting hormone; *PRH,* prolactin-releasing hormone; *CRH,* corticotropin-releasing hormone; *FSH,* follicle-stimulating hormone; *LH,* luteinizing hormone; *TSH,* thyroid-stimulating hormone; *ACTH,* adrenocorticotropic hormone; T₃, triiodothyronine; T₄, thyroxine.

TABLE 19-1

Hormones of the Hypothalamus

HORMONE	SOURCE	TARGET	PRINCIPAL ACTION
Growth hormone-releasing hormone (GHRH)	Hypothalamus	Adenohypophysis (somatotrophs)	Stimulates secretion (release) of growth hormone
Growth hormone-inhibiting hormone (GHIH), or somatostatin	Hypothalamus	Adenohypophysis (somatotrophs)	Inhibits secretion of growth hormone
Corticotropin-releasing hormone (CRH)	Hypothalamus	Adenohypophysis (corticotrophs)	Stimulates release of adrenocorticotropic hormone (ACTH)
Thyrotropin-releasing hormone (TRH)	Hypothalamus	Adenohypophysis (thyrotrophs)	Stimulates release of thyroid-stimulating hormone (TSH)
Gonadotropin-releasing hormone (GnRH)	Hypothalamus	Adenohypophysis (gonadotrophs)	Stimulates release of gonadotropins (FSH and LH)
Prolactin-releasing hormone (PRH)	Hypothalamus	Adenohypophysis (corticotrophs)	Stimulates secretion of prolactin
Prolactin-inhibiting hormones (PIH)	Hypothalamus	Adenohypophysis (corticotrophs)	Inhibits secretion of prolactin

Through negative feedback mechanisms, the hypothalamus adjusts the secretions of the adenohypophysis, and the adenohypophysis adjusts the secretions of its target glands, which in turn adjust the activity of their target tissues (Box 19-3). For example, Figure 19-6 shows the negative feedback control of the secretion of TSH and thyroid hormone (T₃ and T₄).

Box 19-3

HEALTH matters

Clinical Evidence of Feedback Control

Clinical facts provide interesting evidence about feedback control of hormone secretion by the anterior pituitary gland and its target glands. For instance, patients who have the pituitary gland removed (hypophysectomy) surgically or by radiation must be given hormone replacement therapy for the rest of their lives. If not, they will develop thyroid, adrenal cortical, and gonadotropic deficiencies—deficiencies of the anterior pituitary’s target gland hormones. Another well-known clinical fact is that estrogen deficiency develops in women between 40 and 50 years of age. By then the ovaries seem to have tired of producing hormones and ovulating each month. They no longer respond to FSH stimulation, so estrogen deficiency develops, brings about menopause, and persists after menopause. What therefore would you deduce is true of the blood concentration of FSH after menopause? Apply the principle that a low concentration of a target gland hormone stimulates tropic hormone secretion by the anterior pituitary gland and you will understand that FSH levels rise, indeed, after menopause.

Hormone secretion can occur in pulses or peaks, as we see in a graph of minute by minute variations in GH secretion (Figure 19-7). The peaks result from many somatotroph cells in the pituitary collectively increasing their rate of secretion of GH. Such increases result from pulses in GHRH secretion by the hypothalamus (see Figure 19-5), which are especially large during sleep. Exercise, stress, and high-protein meals can cause an increase in the frequency of these peaks.

FIGURE 19-7 **Secretion of growth hormone (GH).**

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Tags: Anthonys Textbook of Anatomy _ Physiology

May 25, 2016 | Posted by admin in ANATOMY | Comments Off