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Chapter 550 Hormones of the Hypothalamus and Pituitary
John S. Parks, Eric I. Felner
The pituitary gland is the major regulator of an elaborate hormonal system. The pituitary gland receives signals from the hypothalamus and responds by sending pituitary hormones to target glands. The target glands produce hormones that provide negative feedback at the level of the hypothalamus and pituitary. This feedback mechanism enables the pituitary to regulate the amount of hormone released into the bloodstream by the target glands. The pituitary’s central role in this hormonal system and its ability to interpret and respond to a variety of signals has led to its designation as the “master gland.”
The pituitary gland is located at the base of the skull in a saddle-shaped cavity of the sphenoid bone called the sella turcica. The bony structure protects and surrounds the pituitary bilaterally and inferiorly. The dura, a dense layer of connective tissue, forms the roof of the sella. An external layer of the dura continues into the sella to form its lining. As a result, the pituitary is extradural and is not normally in contact with cerebrospinal fluid. The pituitary gland is connected to the hypothalamus by the pituitary stalk. The pituitary gland is composed of an anterior (adenohypophysis) and a posterior (neurohypophysis) lobe. The anterior lobe constitutes about 80% of the gland.
The anterior pituitary gland originates from the Rathke pouch as an invagination of the oral ectoderm. It then detaches from the oral epithelium and becomes an individual structure of rapidly proliferating cells. By 6 wk of gestation, the connection between the Rathke pouch and the oropharynx is completely obliterated, and the pouch establishes a direct connection with the downward extension of the hypothalamus, which gives rise to the pituitary stalk. Persistent remnants of the original connection between the Rathke pouch and the oral cavity can develop into craniopharyngiomas, the most common type of tumor in this area.
The arterial blood supply of the pituitary gland originates from the internal carotid via the inferior, middle, and superior hypophyseal arteries. This network of vessels forms a unique portal circulation connecting the hypothalamus and pituitary. The branches of the superior hypophyseal arteries penetrate the stalk and form a network of vessels that traverse the pituitary stalk and terminate in a network of capillaries within the anterior lobe. It is through this portal venous system that hypothalamic hormones are delivered to the anterior pituitary gland. Anterior pituitary hormones, in turn, are secreted into a secondary plexus of portal veins that drain into the dural venous sinuses.
A series of sequentially expressed transcriptional activation factors directs the differentiation and proliferation of anterior pituitary cell types. These proteins are members of a large family of DNA-binding proteins resembling homeobox genes. The consequences of mutations in several of these genes are evident in human forms of multiple pituitary hormone deficiency. Five cell types in the anterior pituitary produce 6 peptide hormones. Somatotropes produce growth hormone (GH), lactotropes produce prolactin (PRL), thyrotropes make thyroid-stimulating hormone (TSH), corticotropes express pro-opiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), and gonadotropes express luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
Human GH is a 191-amino-acid single chain polypeptide that is synthesized, stored, and secreted by somatotropes in the pituitary. Its gene (GH1) is the first in a cluster of 5 closely related genes on the long arm of chromosome 17 (q22-24). The four other genes (CS1, CS2, GH2, and CSP) have greater than 90% sequence identity with the GH1 gene.
GH is secreted in a pulsatile fashion under the regulation of hypothalamic hormones. The alternating secretion of growth hormone–releasing hormone (GHRH), which stimulates GH release, and somatostatin, which inhibits GH release, accounts for the rhythmic secretion of GH. Peaks of GH occur when peaks of GHRH coincide with troughs of somatostatin. Ghrelin, a peptide produced in the arcuate nucleus of the hypothalamus and in much greater quantities by the stomach, also stimulates GH secretion. In addition to the 3 hypothalamic hormones, physiologic factors play a role in stimulating and inhibiting GH. Sleep, exercise, physical stress, trauma, acute illness, puberty, fasting, and hypoglycemia stimulate the release of GH whereas hyperglycemia, hypothyroidism, and glucocorticoids inhibit GH release.
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