sodium and potassium balance Flashcards
what is the normal plasma osmolarity?
285-295 mosmol/L
Sodium ~ 140 mmol/L chloride ~ 105 mmol/L bicarbonate ~ 24 mmol/L potassium ~ 4 mmol/L Glucose ~ 3-8 mmol/L Calcium ~ 2 mmol/L Protein ~ 1 mmol/L
Sodium most prevalent, and important, solute in the ECF.
what happens if you increase dietary sodium?
increased dietary sodium -> increased total body sodium -> increased plasma osmolarity (but this cant happen because of semipermeable membranes) -> increased water intake and retention -> increased ECF volume -> increased blood volume and pressure
the converse happens with decreased dietary sodium
how does the body regulate sodium intake?
central method:
in euvolaemia (normal conditions):
lateral parabracial nucleus tells the brain it doesnt want more salt, so there is less sodium dietary intake
moderated by cells that respond to serotonin and glutamate
in Na+ deprivation:
lateral parabrachial nucleus increases the bodys appetite for sodium intake
moderated by cells that respond to GABA and opioids
peripheral method:
taste buds
salt specific ones
if you have low body sodium it has a more appetitive effect
high body sodium it has a more aversive effect
where is sodium reabsorbed in the kidney?
67% in the PCT
25% in the thick ascending limb
5% in the DCT
3% in the collecting duct
less than 1% is excreted
bur these are proportions, so if you increase GFR, more will be excreted
what effects glomerular filtration rate?
as arterial blood pressure increases renal perfusion rate increases
so does glomerular filtration rate
but this relationship plateaus at blood pressure of about 100 mm Hg
this is useful in terms of eg. if you are exercising you dont want to lose sodium just because of that
how does sodium effect the macula densa?
the DCT is on close contact/association with the juxta glomerular apparatus
the JGA contains macula densa cells
when tubular sodium increases, there is increase uptake of sodium through the Na-Cl-K cotransporter
that causes the macula densa to release adenosine
adenosine triggers the extraglomerular mesangial cells to contract the smooth muscle cells of the glomerulus
this reduces the blood flow to the glomerulus, reducing the GFR
also triggers renin production (eventually increases blood pressure, but it doesnt have much of an effect on renin production over a long period of time)
to summarise:
High tubular sodium
Increased sodium/chloride uptake via triple transporter
Adenosine release from Macula Densa cells
Detected by extraglomerular mesangial cells
Reduces renin production
Promotes afferent SMC contraction
Reduces perfusion pressure and so GFR decreases
more sodium decreases GFR so less sodium is lost
what is the best way to retain sodium and water?
filter less
we do that by reducing the pressure gradient between the afferent arteriole and the efferent arteriole
reduce pressure in the efferent arteriole so it is more similar to that of the afferent
more blood will just go straight past and not be filtered
so better retention of sodium
what factors increase sodium reuptake in the kidneys?
beta 1 sympathetic activity:
directly contracts the afferent arteriole
it also increases uptake of sodium by the cells of the PCT
it stimulates the cells of the JGA to produce renin
this activates angiotensin II
ANGII also stimulates the cells of the PCT to take up sodium
ANG II also stimulates the production of aldosterone from the adrenals
aldosterone stimulates uptake of sodium in the DCT and the collecting duct
low tubular sodium also stimulates the production of renin which also stimulates ANG II production
what factors decrease sodium reuptake in the kidneys?
atrial naturietic peptide;
acts as a vasodilator in the afferent arteriole so higher GFR
reduces sodium reuptake in the PCT, DCT and collecting duct
it surpresses the production of Renin by the JGA
how does bloop pressure and volume affect GFR?
low blood pressure and volume = low GFR
high = high GFR
the lower the GFR the less sodium will be filtered
i think
what is aldosterone?
Steroid hormone
Synthesised and released from the adrenal cortex (zona glomerulosa)
Released in response to Angiotensin ll
stimulated by a Decrease in blood pressure (via baroreceptors)
angiotensin II promotes the synthesis of aldosterone synthetase
aldosterone synthase causes the last two steps of aldosterone synthesis from cholesterol
aldosterone is then released and has its function in the kidney
what is the function of aldosterone?
Stimulates: Increased Sodium reabsorption (controls reabsorption of 35g Na/day) Increased Potassium secretion Increased hydrogen ion secretion
Aldosterone excess:
leads to hypokalaemic alkalosis
how does aldosterone work?
it is a steroid hormone, so lipid soluble
it can pass through the cell membrane
aldosterone binds to the mineralocorticoid receptor in the cytoplasm. this receptor is also bound to a protein called HSP 90. HSP 90 is removed once aldosterone binds
two molecules aldosterone-mineralocorticoid receptor complexes form a Dimer
this allows the complex to translocate into the nucleus, bind to DNA, stimulates the production of mRNA for genes that are under its control including:
the epithelial sodium channel (ENaC)
the sodium potassium ATPase
regulatory proteins that stimulate the activity of these two transporters
so not only more sodium channels but more active as well
what is hypoaldosteronism?
Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium
ECF volume falls Increased renin, Ang II and ADH -> Dizziness Low blood pressure Salt craving palpitations
(addisons?)
what is hyperaldosteronism?
Reabsorption of sodium in the distal nephron is increased
reduced urinary loss of sodium
ECF volume increases (hypertension) reduced renin, Ang II and ADH Increased ANP and BNP -> High blood pressure Muscle weakness Polyuria thirst
what is Liddle’s syndrome?
An inherited disease of high blood pressure.
mutation in the aldosterone activated sodium channel.
- channel is always ‘on’
- Results in sodium retention, leading to hypertension
looks like hyperaldosteronism
but people have normal or low aldosterone
