Regulation of extracellular osmolarity Flashcards
Regulation of extracellular fluid
-critical for cells
-Na is most common ion in ECF that needs to be regulated
What mechanisms are involved in regulation of ECF osmolarity?
1.Osmoreceptor-ADH system
2. The thirst mechanism
**failure of either can be compensated for by the other but failure of both would cause significant changes in plasma Na concentration
Why are plasma and ECF considered together?
-their osmolarity and Na concentrations are very close to each other
How is plasma osmolarity changes sensed?
-Through specialized neuronal cells called osmoreceptors that are located in the hypothalamus at AV3V (anteroventral wall of 3rd ventricle)
Osmoreceptor-ADH feedback
1.Osmolarity of ECF/plasma increases, the Na in the ECF will increase resulting in the osmoreceptors shrinking
2.Shrinkage of osmoreceptors fire signal to supraoptic and paraventricular neurons which triggers ADH release
3.ADH produced by neurons are stored in vesicles that are accumulated at nerve endings in posterior pituitary gland
4. ADH is released in the blood and travels to the kidneys and increases permeability of late distal tubules, cortical collecting tubules and collecting ducts to water.
5.ADH increases water reabsorption so that the osmolarity of plasma and ECF is adjusted
Blood brain barrier and osmolarity detection
-less significant barrier in regions involved in sensing the osmotic pressure of plasma which allows solutes to enter the ECF
What signals affect ADH release?
-osmolarity changes
-decreased arterial pressure
-decreased blood volume
Stimuli affecting ADH
Increase ADH:
-nausea
-nicotine
-Morphine
Decrease ADH:
-alcohol
-caffeine
Blood volume effects on ADH
-reduced blood volume stimulates ADH release but if extracellular osmotic pressure is constant, the ADH release in response to reduced volume is slow
-if blood volume stays constant and osmolarity of ECF increases, the ADH release is fast
Why is water intake important?
-we are constantly losing water through evaporations, perspiration, urine and feces
Thirst center
-located at AV3V and anterolateral wall of 3rd ventricle
What causes sensation of thirst?
Methods:
1.increased osmolarity of ECF causes dehydration cells in the thirst center and lead to sensation of thirst
2.decreased arterial pressure also stimulates thirst through Ang II
3.Dryness of mouth and mucus membranes and esophagus stimulates thirst. Drinking can immediately reduce thirst through mechanism even before decreasing extracellular osmolarity
Angiotensin II
-released when there is low arterial pressure and blood volume loss
-enters the thirst centre and directly stimulates the centre for restoring blood pressure and volume
What can reduce thirst?
-gastrointestinal distension
Threshold for drinking
-changes over 2mEq/L in Na concentration lead to activation of thirst signals
Blockage of aldosterone effects
-aldosterone does not lead to significant changes in plasma Na because ADH and thirst mechanisms regulate this
-both aldosterone and angiotensin II increase Na reabsorption but they also increase water reabsorption. Therefore Na concentration does not change although more Na is being reabsorbed by kidneys
Salt appetite
-we have a behavioural drive to ingest more salt when Na is low. Not very important in humans but it is important in herbivores because low Na diet
Salt appetite center location
-located in AV3V
How is salt appetite stimulated?
-by extreme Na deficiencies or decreased blood volume and blood pressure
Eg. Due to Addison’s disease (very low aldosterone that leads to Na excretion)
What determines the osmolarity of the ECF?
-a balance between the intake and output of water and salt. Na excretion is usually adjusted based on intake
Two main types of adjustments for Na and water excretion
1.Intrarenal adjustments (very effective for normal variations for Na intake)
2. Systemic adjustments (more significant under severe changes of Na intake and renal dysfunction)
Intrarenal adjustments
1.changes in GFR
-from tubuloglomerular feedback and myogenic mechanism
2.changes in reabsorption
-glomerulotubular balance mechanism
Systemic adjustments
1.Pressure natriuresis and diuresis
2.Sympathetic nervous system
3.Angiotensin II
4.Aldosterone
5. ADH
Pressure natriuresis and diuresis effect on systemic adjustments
-powerful mechanism for excretion of excess Na and water
-more important with chronic increased BP due to sustained high Na intake
-with chronic high blood pressure, renal compensatory mechanisms are impaired, so natriuresis can help excrete excess Na and water
Steps of pressure natriuresis and diuresis and increased fluid and Na excretion
- increased Na intake
- accumulation of water
- increased in ECF volume
- increase cardiac output
- increase BP
- natriuresis and diuresis= more Na excretion
- decrease in ECF volume
Sympathetic nervous system effect on Na and water excretion
1.reduced blood volume (eg.hemorrhage)
2.increased sympathetic NS
3. increased in arteriole constriction, tubular reabsorption of salt and water, and renin-angiotensin II
4. Leads to increased Na reabsorption and decrease in GFR
Angiotensin II effect on Na and water excretion
1.increased Na intake
2.decrease in renin
3.decrease in angiotensin II
4. decrease in tubular Na reabsorption
Aldosterone effect on Na and water excretion
1.increase Na intake
2.decrease aldosterone
3.increase in Na excretion
Adrenal gland tumours
-can lead to excessive release of aldosterone
-results in increase in Na reabsorption but when excess Na causes increased arterial pressure, the kidneys escape from further reabsorption of Na under the effect of aldosterone
ADH
*allows kidneys to concentrate urine without changing solute excretion
Excessive ADH effect on Na and water excretion
1.excessive ADH released
2.increase arterial pressure
3.excretion of Na and water (natriuresis and diuresis)
4.extracellular fluid is adjusted but excessive Na excretion
Problem with ADH release
Results in increase in urine (5-10 fold)
-needs to be adjusted by ingestion of more water
