Antidiuretic hormone, or ADH, is a peptide hormone that is anti- or against -diuresis which is excessive urine production. Antidiuretic hormone is also
called vasopressin because it causes vasoconstriction - constriction of blood vessels.So antidiuretic hormone prevents making too much urine, which leads to water retention, and vasoconstriction, and together these two actions help increase the blood pressure.
Now, the brain has two interconnected structures: the hypothalamus and the pituitary gland. These two structures are connected by the pituitary stalk.
The hypothalamus is a part of the brain that contains several nuclei, or clusters of neurons. And two of these nuclei, the paraventricular and supraoptic nuclei, contain neurons that secrete ADH. When ADH is produced, it travels down the axons of these neurons, and these axons have small dilations called Herring bodies, which is where ADH is stored.
Increased plasma osmolarity is the most important physiologic stimulus for increasing antidiuretic hormone secretion. For example, when a person is deprived of water, serum osmolarity increases. The increase is sensed by osmoreceptors in the anterior hypothalamus. Action potentials are initiated in cell bodies of the nearby antidiuretic hormone neurons and propagated down the axons, causing the secretion of antidiuretic hormone from nerve terminals in the posterior pituitary.
Hypovolemia is also a potent stimulus for ADH secretion. Decreases in extracellular fluid volume of 10% or more cause a decrease in arterial blood pressure that is sensed by baroreceptors in the left atrium, carotid artery, and aortic arch. This information about blood pressure is transmitted to the hypothalamus, which directs an increase in ADH secretion.
ADH has two actions, one on the kidney and the other on
vascular smooth muscle.
The major action of ADH is to increase the water permeability of principal cells in the late distal tubule and collecting duct. ADH travel to the kidneys and act
on vasopressin receptor 2, or AVPR2, which is present in the principal cells of the distal convoluted tubule and collecting ducts of the nephrons. When ADH binds to AVPR2 a G protein inside the cell gets activated which goes on to signal membrane bound adenylyl cyclase to convert ATP to cAMP. Increased cAMP leads to two things; first it signals the cell to produce more water channel proteins called aquaporin 2, which usually sit in vesicles inside the principal cell, and second, it also causes vesicles loaded with aquaporin 2 to fuse with the cell membrane, so that the aquaporin 2 proteins can embed themselves in the apical surface of the cells - the side facing the lumen of the tubule.
These aquaporins ultimately allow water to travel out of the lumen of the tubule and into the cells lining the nephron, and ultimately back into the blood. Just like drinking more water, this dilutes the blood, and returns plasma osmolarity to a normal level.
And second, ADH acts on smooth muscles cells in the arteries causing them to constrict, which increase the peripheral vascular resistance and the blood pressure.
