It is a relatively small molecule (peptide) released by the pituitary gland at the base of the brain.
Vasopressin (ADH) has an antidiuretic action that prevents the production of dilute urine (it is also an antidiuretic).
Vasopressin has a vasopressor action and can stimulate the contraction of the arteries and capillaries. Hence the name “vasopressin.” Vasopressin is also known as the antidiuretic hormone (ADH).
Vasopressin has two main sites of action: the kidney and the blood vessels.
The primary function of vasopressin in the body is to regulate extracellular fluid volume by regulating the renal manipulation of water. However, it is also a vasoconstrictor and a pressor agent (hence the name “vasopressin”).
ADH acts on renal collecting ducts through V 2 receptors to increase water permeability, leading to decreased urine formation (hence the antidiuretic action of ‘antidiuretic hormone).
This increases blood volume, cardiac output, and blood pressure.
A secondary function of vasopressin is vasoconstriction. ADH binds to V 1 receptors on vascular smooth muscle to cause vasoconstriction through the IP 3 signal transduction pathway and the Rho-kinase pathway, which increases blood pressure.
However, the average physiological concentrations of ADH are below its vasoactive range. However, studies have shown that in severe hypovolemic shock, ADH contributes to the compensatory increase in systemic vascular resistance when ADH release is very high.
Several mechanisms regulate the release of ADH, the most important of which are the following:
Hypovolemia, which occurs during bleeding and dehydration, causes a decrease in atrial pressure.
Specialized stretch receptors within the atrial walls and large veins (cardiopulmonary baroreceptors) that enter the atria slow down when there is a drop in atrial pressure.
Afferent nerve fibers from these receptors form synapses within the nucleus of the medullary tract solitary, which sends fibers to the hypothalamus. This brain region controls the release of ADH from the pituitary.
The firing of the atrial receptor typically inhibits the release of ADH by the posterior pituitary. With hypovolemia or decreased central venous pressure, decreased firing of atrial stretch receptors leads to increased vasopressin release.
Hypotension, which decreases arterial baroreceptor activation, leads to increased sympathetic activity that increases ADH release.
Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate ADH release when osmolarity increases, as occurs with dehydration.
Angiotensin II receptors located in a region of the hypothalamus regulate the release of ADH: an increase in angiotensin II stimulates the release of vasopressin.
Heart failure is associated with what could be seen as a paradoxical increase in ADH. The increased blood volume and atrial pressure associated with heart failure should decrease ADH secretion, but this is not the case.
It may be that sympathetic, and renin-angiotensin system activation in heart failure overrides cardiovascular volume and low-pressure receptors (as well as hypothalamic control of ADH release) and causes increased vasopressin secretion.
However, this increase in ADH during heart failure may contribute to the increased systemic vascular resistance and the increased renal fluid retention that accompanies heart failure.
ADH infusion is sometimes used to treat septic shock. This condition can be caused by a bacterial infection in the blood and the release of bacterial endotoxins such as lipopolysaccharide.
ADH infusion increases systemic vascular resistance and thus raises blood pressure.