Control of Extracellular Osmolarity and Sodium Concentration Flashcards
Sodium most abundant ion
extracellular fluid Range 140 to 145 mEq/Liter Average 142 mEq/Liter
osmolarity Average
300 mOsm/Liter [282 mOsm/Liter – corrected for
interionic attraction] Range 291 to 309 mOsm/Liter [± 2% to 3%]
precise control of sodium and osmolarity important because
they control distribution of water between intracellular and extracellular compartments
Sodium and associated anions (chloride and bicarbonate) account for
94% of all extracellular solute
Glucose and urea contribute
3 to 5% of total osmolarity Urea able to permeate cells easily so exerts little effective osmotic force
Sodium not very permeable so
has big effect on fluid movement between extracellular and intracellular compartments
Plasma osmolarity =
2.1) x (Plasma concentration sodium) Posm = (2.1) x (142 mEq/L) = 298 mOsm/L
Two systems control / regulate extracellular osmolarity and sodium concentration
Osmoreceptor – ADH system Thirst mechanism
Osmoreceptor Cells location, response, impulses, release, which does what?
Located in anterior hypothalamus Cells shrink in response to increased ECF [Na+] (i.e.
increased osmolarity)
As cells shrink, number of impulses sent to other nerve cells in supraoptic nuclei
Impulses passed to posterior pituitary Impulses stimulate release of AHD stored in secretory
granules within nerve endings
Increased [ADH] of blood stimulates increased water permeability in late distal tubules, cortical collecting tubules, and medullary collecting tubules
Osmoreceptor Cells
Increased osmolarity results in increased water permeability which allows
water to be reabsorbed (conserved) while sodium continues to be excreted at normal rate
ADH release is tied into
the arterial baroreceptor reflexes (which respond to changes in blood pressure) and the cardiopulmonary reflexes (which respond to changes in blood volume)
Reflex pathways tied into
hypothalamic nuclei that control ADH production and release
Decreased blood pressure and/or decreased blood volume results in an increase in ADH release
A 15 to 20% reduction in circulating volume produces a
HUGE increase in [ADH]
Circulating volume must decrease approximately 10% before
appreciable change in [ADH]
factors that Increase ADH Release
Increased plasma osmolarity Decreased blood volume Decreased blood pressure Nausea Hypoxia Morphine, Nicotine, Cyclophosphamide
factors that decrease ADH release
increase BV, increase BP, decrease plasma osmolarity, alcohol, clonidine, haloperidol
Thirst center
Anteroventricular region of third cerebral ventricle (AV3V region) (Also promotes ADH release)
Upper portion contains subfornical organ Inferior portion contains organum vasculosum of the lamina terminalis
thirst center located Anterolaterally in
preoptic nucleus
thirst center neurons within area respond to changes in
osmolarity (function like
osmoreceptors)
thirst mechanism stimulated by Na conc. of
2 mEq/Liter higher than normal Thresholdfordrinking
increase thirst
Increased plasma osmolarity Decreased blood volume** Decreased blood pressure** Increased angiotensin II** Dryness of mouth
decrease thirst
Decreased plasma osmolarity iNCREASED BLOOD VOLUME Increased blood pressure Decreased angiotensin II Gastric distention
With both osmoreceptor-ADH and thirst mechanism intake, able to prevent
though sodium intake has increases 6-fold
Even if one system is not functional, other system still maintain the sodium concentration
If both systems fail, there is no other system that can
regulate sodium concentration so sodium concentration will show large swings depending on sodium intake
