Antidiuretic Hormone

ADH (vasopressin) is released primarily in response to increases in plasma osmolarity or decreases in blood volume. It produces its antidiuretic activity in the kidney, causing the cortical and medullary parts of the collecting duct to become more permeable to water, thereby increasing water reabsorption, reducing serum osmolarity, and increasing its volume. It produces this effect by binding to a subset of vasopressin receptors (Table 59.3) called V2 that have relatively high affinity for the hormone. ADH also has actions at sites other than the kidney. V2 receptors also mediate an increase in circulating levels of two proteins involved in blood coagulation: factor VIII and von Willebrand's factor. At higher concentrations, ADH interacts with V1 receptors to cause a general constriction of most blood vessels. It also interacts with V3 (or V1b) receptors to increase ACTH release, although the major control of ACTH release occurs through corticotropin-releasing hormone.

ADH itself is available for injections (Pitressin) but has a half-life of about 15 minutes. Desmopressin (DDAVP) is an analogue without an amino group at the first amino acid and with D-arginine instead of l-arginine. This analogue is more stable and has very little pressor activity. Desmopressin can be given subcuta-neously or nasally, and the effects last for 12 hours.

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