Human Biochemistry, Volume 2 - Murray R. 1993
Biochemistry of Intracellular and Intercellular Communication
Pituitary and Hypothalamic Hormones
Posterior Pituitary Hormones - Antidiuretic Hormone (ADH; Vasopressin)
Regulation of Secretion
Nerve impulses triggering ADH secretion result from various stimulating factors. The primary physiological stimulus is an increase in plasma osmolality. Its effect is mediated by osmoreceptors located in the Hypothalamus, as well as baroreceptors in The Heart and other vascular compartments. Hemodilution (decreased osmolality) exerts the opposite effect. Other stimuli include emotional and physical stress, as well as pharmacological agents such as acetylcholine, nicotine, and morphine. In most cases, enhanced secretion is accompanied by increased synthesis of ADH and neurophysin II, as hormone stores are not depleted in the process. Epinephrine and agents that expand plasma volume suppress ADH secretion; ethanol has a similar effect.
The most physiologically important target Cells for ADH in mammals are the Cells of the distal convoluted tubules and collecting ducts of the Kidney. These tubules traverse the renal medulla, where the extracellular solute osmolality gradient is fourfold higher than that of plasma. The cells of these tubules are relatively impermeable to Water; consequently, in the absence of ADH, urine is not concentrated and can be excreted in volumes exceeding 20 liters per day. ADH increases cellular water permeability and helps maintain osmotic equilibrium between the collecting duct urine and the hypertonic medullary interstitium, thereby restricting urine volume to 0.5–1 liter per day. The luminal (mucosal) membranes of the epithelial cells in these structures contain ADH receptors coupled to adenylate cyclase; the renal tubular effects of ADH are thought to be mediated by cAMP. This physiological action led to the hormone's designation as "antidiuretic." cAMP and phosphodiesterase inhibitors mimic the effects of ADH. In vivo, elevated calcium levels in the fluid bathing the mucosal surface of the tubules inhibit the water-transporting action of ADH (presumably by inhibiting adenylate cyclase, since The Effect of cAMP itself is not diminished). This mechanism may partly account for the polyuria characteristic of patients with hypercalcemia.
Impairments in ADH secretion or action lead to diabetes insipidus, which is characterized by The excretion of large volumes of dilute urine. Primary diabetes insipidus, associated with ADH deficiency, typically results from damage to the hypothalamo-pituitary tract due to a Skull base fracture, tumor, or infection, though it can also be hereditary. In hereditary nephrogenic diabetes insipidus, ADH secretion remains normal, but target cells lose their ability to respond to the hormone, likely due to a receptor defect (see Table 43.2). This hereditary defect differs from acquired nephrogenic diabetes insipidus, which most commonly arises from therapeutic lithium administration in patients with manic-depressive illness. The syndrome of inappropriate ADH secretion is usually linked to ectopic hormone production by various tumors (typically lung carcinomas), but it can also occur with Brain disorders, pulmonary infections, or hypothyroidism. Such secretion is considered inappropriate because ADH is produced at normal or elevated rates despite hypo-osmolality, leading to sustained and progressive hyponatremia with the excretion of hypertonic urine.
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