Regulation of Osmolality

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Regulation of Water Excretion (Defense of Tonicity)[edit]

  • Vasopressin is secreted from the posterior pituitary gland (along with oxytocin)
  • Discharge of neurons containing vasopressin increases and vasopressin secretion occurs when effective plasma osmotic pressure is > 285mOsm/kg, detected by osmoreceptors in the anterior hypothalamus
  • Posterior pituitary hormones are synthesised in cell bodies of magnocellular neurons in the supraoptic and paraventricular nuclei, and transported down the axons of these neurons to the posterior lobe
  • These are neural hormones, because they are secreted into circulation by nerve cells
  • Vasopressin increases permeability of the collecting ducts in the kidney so that water enters the hypertonic interstitium of the renal pyramids
  • The urine becomes concentrated and its volume decreases
  • Water is retained in excess of solute, causing decreased effective osmotic pressure of body fluids
  • Vasopressin also has vasoconstriction effects and neurological effects
  • Vasopressin secretion is also effected by ECF volume - it is increased by low volume and decreased by high volume, mediated by stretch receptors in the vascular system
  • Hypovolaemia and hypotension produced by conditions like haemorrhage release large amounts of vasopressin. The vasopressin osmotic response curve is shifted to the left.
  • The resulting water retention will often cause hyponatraemia, due to sodium being the most abundant osmotically active plasma component
  • Vasopressin release is also brought about by pain, nausea, surgical stress and emotions. Alcohol decreases vasopressin secretion
  • When vasopressin is absent, urine is hypotonic to plasma, urine volume is increased, there is a net water loss, and body fluid osmolality rises
  • The act of drinking causes some decrease in vasopressin, however the majority is due to a decrease in plasma osmolality
  • If water intake exceeds 16ml/min (the maximal urine flow that can be produced during water diuresis), swelling of cells due to uptake of water from hypotonic ECF occurs
  • In severe cases, water intoxication can develop
  • This leads to swelling of brain cells, convulsions, coma and eventually death
  • This can also occur via administration of exogenous vasopressin, surgical trauma causing secretion of endogenous vasopressin, or from administration of oxytocin without monitoring water intake

Clinical Implications

  • Patients who have had surgery may have elevated plasma vasopressin due to pain and hypovolaemia, which can cause low plasma osmolality and dilutional hyponatraemia
  • Diabetes insipidus occurs either due to vasopressin deficiency (central diapetes insipidus) or when kidneys fail to respond to the hormone (nephrogenic diabetes insipidis)
  • Symptoms include polyuria and polydipsia, and it can be fatal if they cannot increase fluid intake
  • Central diabetes insipidus can be caused by neoplasms in the hypothalamus, post-traumatic, idiopathic, as well as other neurological conditions affecting the hypothalamus
  • Nephrogenic diabetes insipidus can be caused by genetic abnormalities in vasopressin receptor or aquaporin genes
  • dDAVP/desmopressin has very high antidiuretic activity but minimal pressor activity, making it useful in treatment of vasopressin deficiency