![]() These neurons express osmoreceptors that are exquisitely responsive to blood osmolarity and respond to changes as little as two mOsm/L. ADH is stored in neurons within the hypothalamus. Hyperosmolar states most strongly trigger its release. ĪDH is the primary hormone responsible for tonicity homeostasis. After achieving water homeostasis, the ADH levels decrease, and AQP2 is internalized from the plasma membrane, leaving the plasma membrane watertight again. Binding to the receptor triggers an intracellular cyclic adenosine monophosphate (cAMP) pathway, which causes phosphorylation of the aquaporin-2 (AQP2). In states of hypovolemia or hypernatremia, ADH is released from the posterior pituitary gland and binds to the type-2 receptor in principal cells of the collecting duct. Several disease states arise when the body loses control of ADH secretion or responds to its presence. ADH primarily affects the ability of the kidney to reabsorb water when present, ADH induces expression of water transport proteins in the late distal tubule and collecting duct to increase water reabsorption. Given its vital role in multiple functions, it is no surprise that ADH is of great clinical significance. ![]() ![]() Science has known it to play essential roles in the control of the body’s osmotic balance, blood pressure regulation, sodium homeostasis, and kidney functioning. Vasopressin or antidiuretic hormone (ADH) or arginine vasopressin (AVP) is a nonapeptide synthesized in the hypothalamus. ![]()
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