Pharmacology
Summary
Anti-diuretic hormone (ADH), also known as vasopressin, is secreted by the posterior pituitary, and is crucial for regulating plasma tonicity through its actions at the collecting duct of the nephron, where it facilitates free water reabsorption. This hormone functions by activating two subtypes of G-protein-coupled receptors: V1 and V2 receptors.
V1 receptors are found on vascular smooth muscle cells and lead to vasoconstriction and increased blood pressure. V2 receptors trigger the translocation of aquaporin 2 channels, which promote water reabsorption in renal tubule cells. They are also located outside the kidneys, where they regulate the secretion of coagulation factor VIII and von Willebrand factor.
Problems with ADH function can give rise to diseases like diabetes insipidus, which is categorized as either central or nephrogenic. Central diabetes insipidus occurs due to the insufficient production or release of ADH, resulting in decreased circulating ADH, while nephrogenic diabetes insipidus arises when the kidneys do not respond to ADH. Both can be treated using specific methods; for example, the desmopressin acetate (DDAVP), a synthetic analog of ADH, is used in the treatment of central DI, while lithium or thiazide diuretics are used to treat nephrogenic DI.
Syndrome of Inappropriate ADH (SIADH) refers to the overproduction of ADH, which leads to excess water retention and hyponatremia. It can be managed using V2 receptor antagonists, like conivaptan and tolvaptan, and ADH activity interceptor demeclocycline.
Lesson Outline
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FAQs
ADH, or Antidiuretic hormone, is a peptide hormone also known as vasopressin. Produced in the hypothalamus and stored in the pituitary gland, its primary function is to conserve body water by reducing urine output. It works by increasing the permeability of the kidney's collecting duct to water, allowing more water to be reabsorbed back into the bloodstream. Vasopressin also has vasopressor properties, and contributes to the regulation of blood pressure.
ADH receptor antagonists, like conivaptan and tolvaptan, work by blocking the action of ADH on its receptors in the collecting ducts of the kidney. This increases water excretion and decreases urine osmolality, making them relevant in treating hyponatremia and conditions like the Syndrome of Inappropriate ADH (SIADH) where there is an excessive release of ADH.
DDAVP, or desmopressin acetate, is a synthetic analogue of vasopressin that primarily acts on V2 receptors in the kidneys to increase water reabsorption. It is used in the management of conditions such as central diabetes insipidus, von Willebrand disease, and nocturnal enuresis, where increased V2 receptor activation is beneficial.
Disruptions in ADH production, release, or the functioning of ADH receptors can lead to conditions such as diabetes insipidus or the syndrome of inappropriate ADH (SIADH). In diabetes insipidus, deficient ADH or insensitivity of the kidneys to ADH leads to polyuria and polydipsia. In SIADH, excessive release of ADH results in water retention and hyponatremia.
Rapid correction of hyponatremia can lead to a dangerous condition known as central pontine myelinolysis (CPM). This is a type of brain damage that occurs when sodium levels in the blood are increased too quickly. Symptoms may include difficulty speaking, swallowing, and unsteady movements. It's essential to correct hyponatremia slowly to avoid this potentially fatal complication.
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