Vasopressin is a nonapeptide hormone synthesized in magnocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus, which is stored and released from neurosecretory vesicles in the posterior pituitary gland.
The primary physiologic action of vasopressin is its function in water retention. This is accomplished via binding of V2 receptors leading to increased transcription and insertion of aquaporin-2 water channels into the apical membrane of the distal convoluted tubule allowing increased water reabsorption into the medullary circulation and concentration of the urine. Plasma osmolarity is the primary stimulus for secretion under normal physiologic conditions and sodium concentration is the most important contributor to plasma osmolarity. There is a linear relationship between plasma osmolarity and plasma vasopressin concentration with changes in osmolarity as small as 1-2% altering the release of vasopressin. The major sensors of these changes are osmoreceptors in and around the hypothalamus that rapidly respond to osmolarity alterations and consequently increase or decrease secretion of vasopressin from the supraoptic nuclei.
A second major physiologic action of vasopressin is its ability to maintain blood pressure and intravascular volume. These actions are mediated through V1a receptors in vascular smooth muscle with more prominent effects in the capillaries, arterioles, and venules. The first stimulus for causing increased vasopressin secretion for this purpose is decreased blood volume. This stimulus occurs strongly when blood volume decreases greater that 15 to 25 percent. Additionally, stretch receptors in the atria respond to over and under filling leading to reciprocal changes in vasopressin release. Baroreceptors in the carotid, aortic, and pulmonary regions also stimulate vasopressin release when they experience decreased stretching. Of note, the blood pressure effects of vasopressin are minimal in a normal healthy patient and much more pronounced in pathological states such as hypovolemic shock.
Other stimuli for increased vasopressin secretion are nausea, hypoxia, and exercise as well as certain drugs including morphine, nicotine, and cyclophosphamide. Conversely, alcohol, clonidine, and haloperidol all decrease vasopressin secretion. Certain emotional states have also been implicated in affecting vasopressin release.
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