Many of the causes of ADH release are seen post op and with poor fluid management hyponatraemia and transient SIADH can occur
- ADH is a nonapeptide (9 peptide) hormone
- Produced by neurons of the supraoptic and paraventricular nuclei in the hypothalamus
- It is stored and released from the posterior pituitary
- It acts on the collecting ducts improving water permeability and hence water retention.
Stimuli to release
- Increase in osmolality in the plasma perfusing the hypothalamic osmoreceptors
- Low volume in atrial stretch receptors
- Low pressure in arterial baroreceptors
- Angiotensin II, Pain, stress and sleep, Morphine
- Sensation of thirst.
- Increases free water reabsorption in the collecting ducts of the kidney.
- Causes arteriolar contraction
- Raises Blood pressure (Vasopressor)
- Reduces Osmolality
Pathology SIADH (Excess ADH)
- Presents as hyponatraemia and reduced plasma osmolality
- Cell volume is very dependent on the Osmolality changes between ECF and ICF.
- Over release can lead to a fall in serum osmolality
- A fall in ECF osmolality results in cell swelling and e.g. brain swelling
- Cells can address this situation in the case of cell swelling by getting rid of intracellular solutes
Pathology of Diabetes Insipidus
- Polyuria and polydipsia
- Presents as hypernatraemia and increased plasma osmolality
- A loss of ADH release = Cranial DI
- Loss of renal response to ADH = Nephrogenic DI
- Vasopressin has also been used as an agent in cardiac arrest instead of Adrenaline [US Epinephrine] with mixed results
- In synthetic form may be administered as a nasal spray to treat enuresis
- In synthetic form may be administered as a nasal spray to treat Cranial diabetes insipidus