Antidiuretic Hormone (ADH) Physiology
- Antidiuretic Hormone (ADH) is a peptide hormone secreted by the posterior pituitary in response to rising ECF osmolarity or profound hypovolemia. The hormone acts at two basic sites: 1) On the kidneys to enhance a variety of processes that enhance urine concentration, and 2) On the vasculature, triggering vasoconstriction and thus boosting the systemic vascular resistance.
- ADH is synthesized by neurons whose cell bodies reside primarily in the supraoptic nuclei of the hypothalamus. Stimulation of these cell bodies results in release of ADH from their nerve endings which reside in the posterior pituitary.
- Release of ADH is typically controlled by the osmolarity of extracellular fluids. Physiological experiments suggest that neurons within the hypothalamic supraoptic nuclei possess osmoreceptors which directly sense extracellular osmolarity and subsequently modulate the activity of an anatomically adjacent population of ADH-synthesizing neurons. Decreased ECF Osmolarity reduces ADH secretion whereas increased ECF osmolarity increases ADH secretion. While ECF osmolarity is the major modulator of ADH secretion in most cases, in contexts of profoundly decreased effective circulating volume ADH is released by the posterior pituitary independent of the status of osmolarity. These topics are covered in greater detail under ECF Osmoregulation.
- Renal Effects
- ADH acts on the kidneys to enhance a number of processes that concentrate the urine (See: ECF Osmoregulation). This includes increasing the water-permeability of the late distal tubule and collecting duct by promoting placement of aquaporins on principal cell membranes. Additionally, ADH enhances the size of the Corticopapillary Osmotic Gradient responsible for generating the osmotic driving force for water resorption by the late distal tubule and collecting duct. By promoting urine concentration ADH yields net free water resorption to the extracellular fluid and thus dilution of the ECF.
- Vascular Effects
- ADH is a potent vasoconstrictor and and can profoundly increase the systemic vascular resistance, thus explaining the hormone's original name: Vasopressin.