Vasopressin secretion: Control
Basic, Organ-Based and Clinical Sciences
Vasopressin (Arginine vasopressin (AVP) or Anti-diuretic hormone(ADH)) is a peptide hormone made in the supraoptic and paraventricular nuclei of the anterior hypothalamus and is released by posterior pituitary gland in response to particular triggers as detailed below. It acts on the collecting ducts (V2-receptors) to increase permeability, leading to increased water reabsorption. It also increases NaCl reabsorption from the thick ascending limb, which maintains hypertonicity and facilitates water movement out of the collecting ducts. The main effects of vasopressin are net free water retention, increased urine osmolality, and decreased plasma osmolality. It has no direct effect on electrolyte levels and has a short half-life of between 5-15 minutes.
Vasopressin release is controlled by a number of different factors including:
Secretion is regulated by hypothalamic osmoreceptors that respond to increased plasma osmolality (as little as 1% above mOsm/kg). Vasopressin secretion increases with increases in osmolality to increase free water reabsorption thus lowering plasma osmolality.
Mechanoreceptors in the left atrium and pulmonic veins sense changes in intravascular volume, which can stimulate ADH secretion. A reduction of 7-25% of intravascular volume stimulates ADH secretion via vascular mechanoreceptors. Mechanoreceptors are less sensitive than osmoreceptors.
Systemic arterial hypotension, regulated by aortic and carotid baroreceptors, is the most potent trigger of AVP release. Hypotension can cause AVP concentrations of 10-1000 times greater than normal. At these elevated concentrations AVP can act as a vasoconstrictor particularly in the outer renal cortex via the V1a receptor. This receptor exists on vascular smooth muscle, glomerular mesangial cells, and the vasa recta and promotes vasoconstriction. Furthermore, AVP maintains GFR as it is a potent vasoconstrictor of the efferent arteriole.
Additional factors that increase ADH secretion by activating cholinergic neurotransmitters in the hypothalamus:
• Stress- via cortical input can override osmotic/volumetric sensors
• Drugs (chloroform & morphine)
Additional factors that decrease ADH secretion: