Vasopressin (arginine vasopressin, AVP; antidiuretic hormone, ADH) is a nonapeptide hormone formed in the hypothalamus and released from the posterior pituitary. Its primary function in the body is to regulate extracellular fluid volume by affecting renal handling of water; however, it also is a potent vasoconstrictor.
There are several mechanisms regulating the 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 nerve fibers from these receptors synapse within the nucleus tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region of the brain that controls AVP release by the pituitary. 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 principal sites of action: the kidney and blood vessels. The most important physiological action of AVP is to increase water reabsorption in 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 and it acts through vasopressin type 2 (V2) receptors coupled to adenylyl cyclase. AVP also constricts arterial blood vessels by binding to V1 receptors, which are coupled to the Gq-protein and the phospholipase C/IP3 signal transduction pathway. Normal physiological concentrations of AVP are below its vasoactive range; however, in hypovolemic shock when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance.
There are several mechanisms regulating the 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 nerve fibers from these receptors synapse within the nucleus tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region of the brain that controls AVP release by the pituitary. 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 principal sites of action: the kidney and blood vessels. The most important physiological action of AVP is to increase water reabsorption in 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 and it acts through vasopressin type 2 (V2) receptors coupled to adenylyl cyclase. AVP also constricts arterial blood vessels by binding to V1 receptors, which are coupled to the Gq-protein and the phospholipase C/IP3 signal transduction pathway. Normal physiological concentrations of AVP are below its vasoactive range; however, in hypovolemic shock when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance.
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