Water and Salt Metabolism
Osmolality
- Def: concentration of all the solutes in a given weight of water
- Estimation: Posm= 2[Na] + Glucose/18 + BUN/2.8
- Effective solutes: impermeable to cell membranes (i.e. Na+, mannitol) and
therefore restricted to ECF compartment
- create osmotic pressure gradients across cell membranes
- osmotic mov’t of H2O from ICF to ECF compartments
- see
Osmolar Gap
Water Metabolism
- Represents a balance between the intake and excretion of water.
- “Regulated” and “Unregulated” components of regulation
Thirst
- response to perceived deficits of body fluids
- increased osmolality of ECF (threshold: 1-4% increases in plasma
osmolality above basal levels)
- osmoreceptors in anterior hypothalamus
- intravascular hypovolemia (losses of ECF)
- low/high pressure baroreceptors
- circulating angiotensin II (during more severe hypovolemia)
Arginine Vasopressin (A.K.A. Anti-Diuretic Hormone)
- primary regulation of free water excretion by regulation of urinary flow
- Synthesized in hypothalamus
- Supraoptic nucleus
- Paraventricular nucleus
- Transported to/stored in posterior pituitary
- normal pituitary stores allow for > 1week maximal antidiuresis under
sustained dehydration
- AVP acts on the collecting tubules to promote water reabsorption
Regulation of AVP Secretion
- Osmolality
- osmotic threshold: changes of </= 1% plasma osmolality cause increase in
AVP
minute-to-minute regulation b/c of short t ˝of AVP
- the AVP threshold for regulation is much lower than the thirst threshold
- Hypovolemia
- less effect than osmolality-osmolality represents a more sensitive
regulatory system for water balance than does blood or ECF volume
- Nausea (with/without vomiting)
- most potent stimulus to AVP secretion known to man
- not significantly involved in determining physiologic regulation of AVP
secretion
Sodium Metabolism
- Ensures maintenance of ECF volume
- directly supports blood volume and pressure
- Simple balance between intake and excretion of Na+
Renal Sodium Excretion
- Glomerular filtration rate
- decreased GFR= decreased Na+ excretion
- tubuloglomerular feedback
- compensates for changes in filtered load-as filtered load of
Na+increases, Na+absorption by proximal tubule also increases
- Aldosterone
- increases Na+re-absorption in the distal nephron(with exchange for K+)
- Stimulation for secretion:
- renin-angiotensinsystem (angioII)-in response to renalhypoperfusion
- elevated levels of K+
- Inhibition of secretion:
- atrial natriuretic peptide (ANP)
- hyperosmolality
- Other factors
- angiotensin II
- AVP
- ANP
- dopamine
- renal sympathetic nerve activity
- renal prostoglandins
Hyperosmolality and Hypernatremia
- deficiency of water relative to solute in the ECF
- indicates deficiency of TBW relative to total body solute
- most cases due to losses of body water in excess of body solutes
Pathogenesis of hyperosmolar disorders
- Assessment for Renal Cause
- Urine osmolality
- appropriately concentrated urine usually eliminates possibility of
primary renal cause
- urine osm >800 mOsm/kg H20= nml AVP secretion and renal response
- urine osm <800mOsm/kg H2O= presence of renal concentrating defect
- always check urine for glucose
- in absence of osmotic diuresis, inadequate urine concentration generally
indicates presence of Diabetes insipidus
see SIADH,
Diabetes Insipidus