The posterior pituitary, or neurohypophysis, is composed of modified glial cells (termed pituicytes) and axonal processes extending from nerve cell bodies in the supraoptic and paraventricular nuclei of the hypothalamus. The hypothalamic neurons produce two peptides: antidiuretic hormone (ADH) and oxytocin. They are stored in axon terminals in the neurohypophysis and released into the circulation in response to appropriate stimuli. Oxytocin stimulates the contraction of smooth muscle in the pregnant uterus and those surrounding the lactiferous ducts of the mammary glands. Abnormal oxytocin synthesis and release has not been associated with significant clinical abnormalities. The clinically important posterior pituitary syndromes involve ADH production. They include diabetes insipidus and secretion of inappropriately high levels of ADH.
ADH is a nonapeptide hormone synthesized predominantly in the supraoptic nucleus. In response to several different stimuli, including increased plasma oncotic pressure, left atrial distention, exercise, and certain emotional states, ADH is released from axon terminals in the neurohypophysis into the general circulation. The hormone acts on the collecting tubules of the kidney to promote the resorption of free water. ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria) caused by an inability of the kidney to properly resorb water from the urine. Diabetes insipidus can result from several causes, including head trauma, neoplasms, and inflammatory disorders of the hypothalamus and pituitary, and from surgical procedures involving the hypothalamus or pituitary. The condition sometimes arises spontaneously (“idiopathic”) in the absence of an underlying disorder. Diabetes insipidus from ADH deficiency is designated as central, to differentiate it from nephrogenic diabetes insipidus as a result of renal tubular unresponsiveness to circulating ADH. The clinical manifestations of both diseases are similar and include the excretion of large volumes of dilute urine with an inappropriately low specific gravity. Serum sodium and osmolality are increased as a result of excessive renal loss of free water, resulting in thirst and polydipsia. Patients who can drink water can generally compensate for urinary losses; patients who are obtunded, bedridden, or otherwise limited in their ability to obtain water may develop life-threatening dehydration.
In the syndrome of inappropriate ADH (SIADH) secretion, ADH excess is caused by several extracranial and intracranial disorders. It causes resorption of excessive amounts of free water, with resultant hyponatremia. The most common causes of SIADH include the secretion of ectopic ADH by malignant neoplasms (particularly small-cell carcinomas of the lung), non-neoplastic diseases of the lung, and local injury to the hypothalamus and/or neurohypophysis. The clinical manifestations of SIADH are dominated by hyponatremia, cerebral edema, and resultant neurologic dysfunction. Although total body water is increased, blood volume remains normal and peripheral edema does not develop.