Renal regulation of ECF osmolarity and volume Flashcards
Why is ECF osmolarity strictly controlled
- to guard against changes in ICF composition
ECF loss results in what
increase in osmolarity = cells shrink
ECF gain results in what
decrease in osmolarity = cells swell
Describe what regulates ECF osmolarity and volume ( 5 )
1- ADH 2- Aldosterone 3- RAAS 4- Atrial natriuretic peptide 5- Thirst
Explain the mechanism by which ADH is secreted with Hypertonic ECF ( <280 )
- osmoreceptor neurons in hypothalamus have aquaporin channels that allow water to exit cell when ECF is hypertonic
- shrinking of osmoreceptor neurons opens stretch sensitive channels
- calcium and sodium enters causing depolarisation
- action potential passes down to supra optic and paraventricular neurons
- ADH is released from posterior pituitary
What are the effects of ADH secretion
- increased water reabsorption at DCT and collecting duct
- ADH inserts aquaporin channels into walls of DCT and Collecting duct to allow water back into blood
- dilutes plasma
Explain the mechanism by which ADH is secreted with Hypotonic ECF ( >280 )
- aquaporin channels allow water to enter cell by osmosis
- osmoreceptors expand causing stretch channels to be inactivated
- decrease in Ca and NA result in no depolarization and no action potential
- no signal is sent for ADH release
What are the effects of no ADH secretion
- no reabsorption of water at DCT and CD
- ECF osmolarity increases
- dilute urine
Explain the mechanism by which ADH is secreted due to Blood pressure increase
- Baroreceptors in carotid sinus and aortic arch sense stretch of blood vessel wall
- baroreceptors activate with every heart beat and cause Ca and Na to enter and depolarize the nerve cell
- signal sent up to hypothalamus
- Inhibiting Supra optic and Paraventricular release of ADH
- decrease water reabsorption = decrease BP
Explain the mechanism by which ADH is secreted due to Blood pressure decrease
- signals sent to hypothalamus from baroreceptors are reduced
- ADH release is increased by supra optic and paraventricular
- increasing water reabsorption = increase BP
Explain the mechanism by which Aldosterone is secreted to hyperkalaemia
- mineralocorticoids are released by zona glomerulosa
- K is reabsorbed in PCT, Asc Loop, DCT and CD
- triggers aldosterone which increases expression of Na K pump in DCT and CD
- increasing Na reabsorption and K secretion
What causes release of aldosterone ( 4 )
1- increase of K in plasma
2- Increase of ACTH, AngII
3- decrease of plasma PH
4- decrease of atrial stretch , BP
Explain the result of Aldosterone on ECF
-increase of sodium reabsorption = increase of water reabsorption and K secretion to urine
What are the results of Hyperaldosteronism
- Hypertension and Hypokalemia
How is Hyperaldosteronism treated
- treated by surgery or aldosterone antagonist
What are the causes of Hypoaldosteronism
1- primary, secondary , tertiary adrenal insufficiency
2- congenital adrenal hyperplasia
3- medications
What are the results of Hypoaldosteronism
- Hyperkalaemia : palpitations , muscle pain , abnormal heart rhythm , cardiac arrest
What is isolated hypoaldosteronism
- reduced production of aldosterone without corresponding changes in cortisol
What is used to differentiate between the causes of hypoaldesteronism in patient
- ACTH release is stimulated
- if low aldosterone release then primary hypoaldestornism
- if large aldosterone release then secondary hypoaldosteronism
Explain the mechanism by which RAAS is activated due to reduced ECF osmolarity and the result
- Na reabsorption is reduced in DCT
- detected by kidney to cause renin release
- renin enters blood stream causing Angiotensinogen to convert to AngI
- Ang I becomes AngII
- AngII acts on adrenal cortex to cause aldosterone release
- increasing Na reabsorption
- increases water reabsorption
Where else does AngII act on other than adrenal cortex
- acts on brain to stimulate ADH secretion
- increases water reabsorption
- increase BV= increase BP & CO
What three things activate RAAS
- decrease in ECF osmolarity
- increase in SNS
- decrease in Blood pressure
What happens when ECF osmolarity is low and we want an increase in Na reabsorption to increase osmolarity but not an increase in water which would dilute the ECF
- Hypothalamus will override the effects of AngII on ADH release
- decrease ADH release = reduce water reabsorption
What happens due to reduced Na reabsorption to the Juxta-glomerular cells
- PGE2 is activated in juxtaglomerular cells
- results in renin production from them
What happens due to Sympathetic activity to the Juxta-glomerular cells
- increases cAMP
- results in renin production
What happens when blood pressure increases is detected in afferent arteriole
- stretch sensitive channels on Juxta-glomerular cells are activated
- decrease cAMP
- stop renin production
Explain the mechanism by which Atrial Natriuretic Peptide is secreted due to increase in BV and the result
- ANP is released by atrial myocytes in response to atrial distension
- ANP inhibits renin release
- decreases circulating AngII and aldosterone ( natriuresis and diuresis )
- ANP improves GFR = Diuresis
- reduces BV = reduce BP
- ANP also causes vasodilation = decrease in BP
Explain the mechanism by which RAAS is activated due to Sympathetic activity and decrease Blood pressure and the result
- renin enters blood stream causing Angiotensinogen to convert to AngI
- Ang I becomes AngII
- AngII acts on adrenal cortex to cause aldosterone release
- AngII also acts to release ADH which results in increase of water reabsorption
- increasing Na reabsorption
- increases water reabsorption
- increases BV= increase BP & CO
What is the purpose of Natriuretic peptides
- natural counter-regulatory system for RAAS
- useful for hypertension and CHF treatment because it maintains K levels in body
Explain the mechanism by which Thirst is activated by high ECF
- ECF osmolarity increase activates thirst sensors
- increases water consumption
- normalises osmolarity
How is the thirst mechanism separate from ADH ( 3 reasons )
1- Thirst is anticipated ( ex: when you eat )
2- thirst is rapidly suppressed after drinking even if what has driven the thirst is still there
3- threshold for thirst activation is higher than ADH
Where are thirst sensors
- suggested to be anterior cingulate cortex in brain
What activates thirst sensors ( 3 )
1- High ECF osmolarity
2- Bria input ( food )
3- input from body ( dry mouth, hypovalemia )
How do kidney’s know what and how much to eliminate (4 steps ) and what Is the result
1- imbalance in BV/BP or osmolarity produces a stimulus
2- stretch sensors or Na transporters are activated
3- signals are sent to control centres ( hypothalamus , JG apparatus , heart )
4- Effectors released ( renin , aldosterone, ADH release )
5- Natriuresis, Diuresis , water consumption response
What’s the homeostatic mechanism of decrease in ECF osmolarity and decrease in Na ( hint : macula dense )
- Na transporters are activated
- signals sent to Macula Densa
- Increase renin production
- increase Na and H20 reabsorption
Which of these treatments for hypertension are working to RAS or Kidneys
1- Diuertics 2- Calcium channel blockers 3- ACE inhibitors 4- AngII receptor antagonist 5- Beta-adrenergic receptor antagonist 6- Vasodilators 7- Renin inhibitors 8- Aldosterone receptor antagonist 9- Alpha2 adrenergic receptor
1- effect on kidney
2- major effect directly on blood vessels
3- doesn’t allow AngII activation by renin
4- effect kidney
5- affect SNS on renin release
6- major effect directly on blood vessels
7- effect kidney
8- effect kidney
9 -major effect directly on blood vessels
