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Anti-diuretic Hormone (ADH) Physiology
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Anti-diuretic Hormone (ADH) Physiology

Anti-Diuretic Hormone Physiology
Overview
Anti-diuretic hormone, or ADH for short, is also called "arginine vasopressin" (AVP), or, simply, vasopressin. Responsible for regulating body water and blood pressure.
ADH assists aldosterone during hemorrhage or other hypovolemic states – it does this by raising the intravascular volume to maintain tissue perfusion.
    • Thus, ADH is given during hypotensive crisis.
Key pathologies of ADH include:
    • Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH), which occurs when ADH is excessively secreted.
    • Diabetes insipidus, when there is too little secretion of or reaction to ADH.
Anti-Diuretic Hormone Physiology
First, we show the hypothalamus and pituitary and that the anterior pituitary gland comprises clusters of hormone-producing cells. The posterior pituitary comprises neural tissue.
ADH pro-hormones are produced in the supraoptic and paraventricular nuclei of the hypothalamus; on their way to the posterior pituitary, these prohormones are converted to ADH. From there, ADH is secreted into the blood stream and travels to its targets.
Unlike anterior pituitary hormones, the posterior pituitary hormones are not stored until needed; instead, stimulation of the hypothalamic centers triggers their production and secretion on demand.
Two triggers for ADH release:
    • ADH is released in response to minute increases in plasma osmolality (so, above ~ 280 milliosmoles per kilogram of water), for example, in response to hypernatremia.
    • ADH is also released in response to decreases in intravascular pressure, such as in hypovolemia.
Serum Osmolality
Changes in serum osmolality are sensed by hypothalamic osmoreceptors, which triggers the release of ADH.
We show a nephron, and show that ADH binds V2-receptors in the distal nephron, causing the insertion of special water channels called aquaporins.
When ADH is present, the number of aquaporins increases so that more water is reabsorbed from the distal nephron.
    • Because more water is resorbed, urine volume is reduced and its osmolality is increased (in other words, the small amount of urine produced contains a high concentration of solutes).
When osmolality returns to baseline, ADH release stops, and urine production returns to normal.
    • In the absence of ADH, water reabsorption is reduced, so urine volume increases and its osmolality decreases (the larger volume of urine is more dilute).
Blood Pressure
Changes in blood pressure are sensed by baroreceptors in the chest (review baroreceptors).
In response to reduced blood pressure, ADH is released and binds to V1A-receptors in the vascular smooth muscle. ADH causes vasoconstriction, which raises the intravascular blood pressure to maintain tissue perfusion.
Osmolality vs Blood Pressure
    • It takes a higher concentration of ADH to achieve the vascular effects than to achieve the water-balancing effects in the nephron.
    • In hypovolemia, ADH will be released in high quantities, regardless of the osmotic state.
    • In hypervolemia, ADH release will be inhibited, regardless of the osmotic state.
    • In other words, blood pressure homeostasis is prioritized over water balance, which underscores the importance of tissue perfusion.
SIADH Diabetes insipidus

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