Arginine vasopressin: Secretion
Basic, Organ-Based and Clinical Sciences
Arginine vasopressin or antidiuretic hormone (ADH) is a nonpeptide hormone that is essential for volume homeostasis. It is synthesized in the magnocellular neurosecretory neurons in the paraventricular nucleus and supraoptic nucleus of the hypothalamus and transported down the hypothalamoneurohypophyseal tract to be stored in the posterior pituitary gland. The PRIMARY stimulation for secretion of vasopressin is an increase in plasma osmolality. This occurs when there is a decrease in intravascular and extracellular volume leading to solute contraction and increased osmolality. Baroreceptors can also play a role in regulating vasopressin release but this is much less prominent than the osmolality effect.
Vasopressin has several downstream effects. The first is at the V2 receptor in the collecting ducts of the kidney where it opens aquaporin 2 channels, which leads to water reabsorption and urine concentration thus increases intravascular volume. The pores allow water to osmotically move down its concentration gradient from the nephron back into the blood. It also leads to increase sodium retention in the ascending loop of Henle, which further increases the osmotic gradient and leads to more pronounced distal water absorption.
Vasopressin also acts at the V1 receptor, which is located throughout the body, most prominently in the vasculature. Stimulation leads to profound vasoconstriction. This increases afterload in an attempt to increase perfusion throughout the body.
There are also several other things that help control the release and effect of vasopressin. Ethanol reduces vasopressin release and leads to a prodiuretic state with volume loss. Atrial natriuretic peptide also helps to decrease vasopressin release when the atrium is stretched indicating a hyervolemic state. Finally, angiotensin II leads to further release of vasopressin for more pronounced vasoconstriction.