salt and water balance Flashcards
aldosterone site of action
collecting tubule and duct
angiotensin 2 site of action
proximal tubule, thick ascending loop of henle/disal tubule, collecting tubule
ADH
anti diuretic hormone
water loss r regulated by sodium osmolarity
an increase in extra cellular fluid osmolarity causes osmoreceptor cells to shrink, triggering an action potential causing posterior pituitary to release ADH
ADH goes to kidneys to increase water permeability of the DCT/CT.CDs
increased reabsorption of water
H2O is conserved which Na+ solutes continue to be excreted - dilution of ECF solutes
ADH is synthesised in
produced in the supraoptic and paraventricular nuclei in the hypothalamus
stored in the posterior pituitary
ADH is released when
release is triggered by increase in plasma osmolarity
stimulates exocytosis of ADH into the blood stream
what does ADH do
increased water permeability of DCT/CT.CD
retains water
increases aquaporinb activity
aquaporin 2
has two states
- can be endocytose into a vesicle so it is not active
- can be expocytosed and presented to the membrane where it can be open
how does ADH increase aquaporinb activity
- binds V2 receptors > cAMP > kinases > translocation of aquaporin 2 to the luminal membrane where it is active
- aquaporin 2 cluster together, form water channels that permit rapid H2O diffusion
aquaporin 3 and 4
in the basolateral membrane provide a path for water to rapidly exit the cells - not ADH regulated
chronic ADH
alo stimulates aquaporinb 2 transcription
decrease in ADH concentration affect on aquaporinb 2
causes aquaporinb 2 to be endocytosed
renin-angiotensin-aldosterone system
- decrease in renal perfusion - tubuloglomerular feedback - renin is released which converted angiotensinogen to angiotensin 1
- angiotensin 1 has low activity, ACE activates it to angiotensin 2 - high activity, short half life - acts in the systemic circulation and is degraded before it reaches the pulmonary circulation
angiotensin 2 affect on the kidney
- increasing activity of sodium potassium pumps which causes more sodium to be retained
- stimulates release and production of aldosterone
aldosterone affect on the kidney
- increase sodium potassium pump activity and therefore sodium retention
angiotensin 2
high activity, short half life
activated version of angiotensin 1
acts on the systemic circulation and is deactivated before it reaches the pulmonary circulation
renin is secreted by
granular cells of the JGA
renin is secreted due to
catalysed by tubuloglomerular feedback
when there is a decrease in the amount of sodium in the distal collecting tubules
triggers the release of renin into the plasma
renin causes
turns angiotensin 1 to angiotensin2
aldosterone
- secreted by adrenal cortex zona glomerulosa
- secretion is mediated by angiotensin 2 and increased local potassium concentration
aldosterone action in kidney
steroid
diffuses across plasma membrane and binds mineralocorticoid receptor and becomes a transcription factor when activated
changes transcription in cells o produce more sodium potassium pump and sodium channels
ANP
atrial natriuretic peptide
- decreases Na+ and H2o reabsorption
- antagonist of aldosterone and angiotensin
- produced in response to atrial stretch
- inhibits sodium retention mechanism - slows sodium potassium pumps
- increases GFR
ANP affect on GFR
increases
ANP affect on sodium potassium pumps
slows
ANP secreted in response to
atrial stretch - too much venous blood volume
when the atria are stretched
ANP releases
- increases GFR
- decreases renin and aldosterone
- increased sodium and H2O excretion
potassium regulation
lethal - must be controlled/sequestered inside cells
- intracellular fluid is high in potassium
factor that shift K into cells
- insulin
- aldosterone
- beta adrenergic stimulation
- alkalosis
factors that shift K out of cells
- insulin deficiency - diabetes
- aldosterone deficiency - Addison’s disease
- beta adrenergic blockade
- acidosis
- cell lysis
- strenuous exercise
- increased extracellular fluid osmolarity
insulin and adrenaline on potassium
ECF > ICF
cell lysis and muscle damage on potassium
ICF > ECF
potassium secretion
balance of secretion and resorption
regulated section - principle cells (late DCT/CT)
by retaining more sodium, more potassium is lost
secretion rate of potassium is determined by
- Na/K ATPase activity
- K electrochemical gradient
- K permeability
minimally resorbed
K feedback control
local potassium levels are a trigger for aldosterone release - elevated potassium increases aldosterone to stop potassium from being toxic
3 mechanisms of K feedback control
- increase in K stimulates NA K ATPase
- increase in K stimulates increase in K gradient to drive diffusion
- increase in K stimulates aldosterone secretion
drinking threshold is regulated by
sodium
increase in extracellular sodium ECF triggers thirst mechanism
thirst stimuli
- hypertonicity - hypothalamic osmoreceptors which inactivated thirst mechanisms
- hypovolaemia
- hypotension
- angiotensin 2 - potent dipsinogen
all feed into the hypothalamus
osmoreceptors are located in
AV3V region
receive information for medullary blood pressure centres
project to supraoptic and paraventricular nuclei - ADH synthesis
2 primary stimuli for salt appetite
- decrease of ECF sodium - decreases thirst/more hunger for salt
- decrease of blood pressure increases thirst and salt appetite
region that governs salt appetite
AV3V region
