THE MERCK VETERINARY MANUAL
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Overview of the Pituitary Gland

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The pituitary gland (hypophysis) is composed of the adenohypophysis (anterior lobe) and the neurohypophysis (posterior lobe).

The adenohypophysis, which surrounds the pars nervosa of the neurohypophyseal system to varying degrees in different species, consists of the pars distalis, the pars tuberalis, and the pars intermedia. The pars distalis is the largest part and contains multiple populations of endocrine cells. The pars tuberalis functions primarily as a scaffold for the capillary network of the hypophyseal portal system. The pars intermedia forms the junction between the pars distalis and pars nervosa. It contains two populations of cells in dogs, one of which synthesizes adrenocorticotropic hormone (ACTH).

A specific population of endocrine cells in the pars distalis (and in the pars intermedia for ACTH in dogs) synthesizes and secretes each of the pituitary trophic hormones. Pituitary cells have a secretory cycle and enter an actively synthesizing phase in response to increased demand for a particular hormone. Secretory cells in the adenohypophysis are often subdivided into chromophils (acidophils, basophils) and chromophobes based on interaction of the secretory granules with pH-dependent histochemical stains.

Acidophils are further subdivided into somatotrophs that secrete growth hormone (GH, somatotropin) and lactotrophs that secrete prolactin. Basophils include gonadotrophs that secrete both luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and thyrotrophs that secrete thyrotropic hormone (thyroid-stimulating hormone [TSH]). Chromophobes include the endocrine cells involved in the synthesis of ACTH and melanocyte-stimulating hormone (MSH), nonsecretory follicular cells, and undifferentiated stem cells.

Endocrine cells in the adenohypophysis are under the control of corresponding hypothalamic-releasing hormones. These releasing hormones are conveyed by the hypophyseal portal system to specific cells in the adenohypophysis, where they stimulate the rapid release of preformed trophic hormones.

Separate hypothalamic-releasing hormones regulate the rate of secretion of each trophic hormone from the adenohypophysis. For most pituitary trophic hormones, negative feedback control is accomplished by a feedback loop involving the blood concentration of the hormone produced by the target endocrine gland (eg, thyroid gland, adrenal cortex, ovary, and testis). Hormones such as prolactin, GH, and MSH have more complex feedback mechanisms. For example, prolactin affects primarily the mammary gland, and GH has its principal effect on the liver—both nonendocrine tissues. The negative feedback in such cases includes metabolites and other messengers (eg, insulin-like growth factor I produced by the liver). In the case of GH, there is an inhibitory (somatostatin) as well as stimulatory (GH-releasing hormone) hypothalamic regulator.

The neurohypophysis (pars nervosa, posterior lobe) has three anatomic subdivisions. Secretion granules that contain the neurohypophyseal hormones, ie, antidiuretic hormone (ADH, vasopressin) and oxytocin, are synthesized in the hypothalamus but are released into the bloodstream in the pars nervosa. The infundibular stalk joins the pars nervosa to the overlying hypothalamus.

ADH, an octapeptide synthesized in the hypothalamus, is packaged into membrane-limited granules with a corresponding binding protein (neurophysin) and transported to the pars nervosa, where it is released into the circulation. ADH binds to specific receptors in the distal part of the nephron and collecting duct of the kidney; it increases the renal tubular reabsorption of water from the glomerular filtrate.

The output of ADH is directly related to the degree of hydration of the body. Hydration of the body inhibits release of ADH, while dehydration or injection of hypertonic electrolyte solutions favors release of ADH, which in turn causes increased water resorption from the glomerular filtrate, resulting in dilution and decreased osmolarity of body fluids. Barbiturates, ether, chloroform, morphine, acetylcholine, nicotine, and pain increase ADH release, which leads to less urine formation. Ethanol inhibits ADH release, which leads to diuresis.

The pressor effect of ADH is less prominent than the antidiuretic effect. At a dosage several hundred times larger than the antidiuretic dosage, ADH has a pronounced pressor effect, which may also lead to coronary constriction. The contractile mechanism of the capillaries, as well as GI and uterine muscle, is stimulated, and a prolonged increase in blood pressure follows.

Oxytocin has specific effects on the smooth muscle of the uterus and the myoepithelial cells of the mammary gland. It has no established physiologic function in the male, although an effect on sperm transport has been suggested.

Last full review/revision November 2013 by Deborah S. Greco, DVM, PhD, DACVIM

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