Antidiuretic Hormone (ADH, Vasopressin)
Antidiuretic hormone (ADH), or arginine vasopressin (AVP), is a peptide hormone produced by the hypothalamus, and stored in the posterior pituitary gland. ADH acts on the kidneys, concentrating the urine by promoting the reabsorption of water and salt into the cortical collecting duct.
ADH is activated by "water receptors" in both the extracellular fluid volume and the intracellular fluid volume. Ethanol and caffeine block the release of ADH from the posterior pituitary gland. This decrease in water reabsorption leads to a higher volume of urine output. In the extracellular fluid the activators are maily baroreceptors in the veins, atria, and arterioles. In the intracellular fluid the activators are mainly osmoreceptors in the hypothalamus.
Antidiuretic hormone (ADH) is normally produced in the neurohypophysis to regulate plasma osmolality.The characteristic syndrome due to ADH hypersecretion was first described in 1957 by Schwartz.The two key features of this syndrome are hyponatremia with hyposmolarity and inappropriately concentrated urine.Hyponatremia associated with lung malignancy is commonly due to inappropriate secretion of ADH.
There are several mechanisms regulating release of AVP. Hypovolemia, as occurs during hemorrhage, results in a decrease in atrial pressure. Specialized stretch receptors within the atrial walls and large veins (cardiopulmonary baroreceptors) entering the atria decrease their firing rate when there is a fall in atrial pressure. Afferent from these receptors synapse within the hypothalamus; atrial receptor firing normally inhibits the release of AVP by the posterior pituitary. With hypovolemia or decreased central venous pressure, the decreased firing of atrial stretch receptors leads to an increase in AVP release. Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate AVP release when osmolarity rises, as occurs with dehydration. Finally, angiotensin II receptors located in a region of the hypothalamus regulate AVP release – an increase in angiotensin II simulates AVP release.
AVP has two principle sites of action: kidney and blood vessels. The most important physiological action of AVP is that it increases water reabsorption by the kidneys by increasing water permeability in the collecting duct, thereby permitting the formation of a more concentrated urine. This is the antidiuretic effect of AVP. This hormone also constricts arterial blood vessels; however, the normal physiological concentrations of AVP are below its vasoactive range. Studies have shown, nevertheless, that in severe hypovolemic shock, when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance.