Regulation of ECF volume Flashcards
What is the TBW distribution determined by?
number of osmotically active particles in each component
What are the major ECF osmoles?
sodium and chloride
What is the major ICF osmole?
potassium salts
What are the 2 parts of the ECF?
plasma and ISF
fraction distribution of water between ICF and ECF
ECF - 1/3
ICF -2/3
What happens as a result of changes in sodium content of the ECF?
changes in ECF volume which leads to affects on volume of blood perfusing tissues and effective circulating volume and blood pressure
What is sodium regulation dependent on? (hint: what receptors?)
high and low pressure baroreceptors
If excessive salt and water is lost what happens to blood pressure? explain
decrease PV, decrease venous pressure, venous return, atrial pressure, EDD, SV, CO and bp
If there is salt and water loss what do high pressure baroreceptors do?
increase sympathetic VC therefore increasing TPR and bloo dpressure
sympathetic vasoconstriction effects on kidney
renal artery constriction and renin increase
What does renin do?
cleaves angiotensinogen to angiotensin 1
angiotensin 2 - how does it increase bp?
increase sodium and water reabsorption at proximal tubule
What does aldosterone do to increase bp?
increase distal tube reabsorption of sodium and water
How is the changes in proximal tubule sodium reabsorption after vomiting achieved?
changes in rate of uptake by peritubular capillaries determined by oncotic pressure
Why is the oncotic pressure and hence sodium reabsorption increased after vomiting?
sodium and water = wet stuff = lost
How much of sodium and water can be reabsorbed at proximal tubule after vomiting?
75%
Why is GFR unaffected after vomiting? When would it be affected?
autoregulation - constriction of afferent arteriole and angiotensin 2 constriction on efferent
considerable decrease in mean blood pressure
What regulates distal tubule sodium reabsorption?
aldosterone
How is aldosterone secretion controlled?
reflexes involving kidney themselves
What are juxtaglomerular cells?
large epithelial cells of afferent arteriole before it enters the glomerulus with plentiful granules
What is the macula densa?
closely associated loop of distal tubule
JG cells + macula densa =?
juxtaglomerular apparatus
Where is renin produced? in response to..
juxtaglomerular cells
drop in bp
What converts angiotensin 1 –> angiotensin 2?
ACE
Explain the 4 was in which angiotensin 2 increases bp
adrenal cortex to produce aldosterone which increases sodium rebabsorption
arteriolar vasoconstriction
medulla oblongata control centre
Hypothalamus –> ADH and thirst
Where is the enzyme ACE found?
throughout vascular endothelium
greatest proportion in pulmonary circuit
How does angiotensin 2 stimulate aldosterone production?
stimulates aldosterone secreting cells in the zona glomerulosa of the adrenal cortex
Where does aldosterone travel to and what is its effect?
in blood to kidney
increase distal tubule sodium reabsorption
What is the rate limiting step of sodium reabsorption (angiotensin 2 pathway)
renin release as angiotensinogen is always present
List the 5 things which controls renin release
P in afferent arteriole at JG cells decreases
increased sympathetic nerve activity by beta 1 effect
inversely proportional to sodium delivery at macula densa
angiotensin 2 feedback to inhibit renin
ADH inhibits renin release
How do JG cells increase renin release?
“renal baroreceptors”
less distension –> more renin
What is meant by the JG cells renin pathway being an intrinsic property?
occur even if denervated
Is GFR increases explain how it is decreased eg tight control
increased GFR means more fluid in proximal tubule and flow past the macula densa increases which sends paracrine signals to the JG cells to produce renin. afferent arteriole constricts, resistance increases, hydrostatic pressure decreases and GFR decreases
Is osmolarity or ECF volume more important to restore first in an emergency?
volume
What is normally the main determinant of ADH?
osmolarity
What should you do in the case of large salt and water loss and why?
infuse or drink saline
lose salt and water - replace salt and water
Aldosterone and ANP - which increases sodium reabsorption and which increases sodium excretion?
Aldosterone - reabsorption
ANP - excretion
Why would weight gain occur if someone was given aldosterone?
sodium and water retention
After a few days of aldosterone administration what happens?
spontaneous diuresis due to volume expansion and potassium loss
ANP over-rides aldosterone
Is someone with conns depleted of sodium or potassium?
potassium
What secretes ANP and when?
atrial cells
expansion of ECF volume
What does ANP cause?
natriuresis - loss of sodium and water in urine
If blood glucose is uncontrolled in diabetes what happens to glucose in proximal tubule?
persists as exceeded TM
What does glucose excess in proximal tubule result in?
water retention in tubule which dilutes contents
Why is sodium reabsorption decreased in hyperglycaemia? Knock on effect of this?
concentration gradient decreased as sodium in lumen diluted
glucose shares symport - not reabsorbed
In hyperglycaemia why is the fluid not as concentrated in descending limb?
sodium and glucose exert osmotic efflux on water to retain it
Why is sodium reabsorption in distal tubule decreased in hyperglycaemia?
macula densa senses large volume in distal tubule
renin is suppressed
Why is ADH ability to conserve water abolished in hyperglycaemia? Why is it stimulated in the first place?
interstitial gradient wrecked
losing a lot of fluid - ADH stimulated via baroreceptors as change in volume not osmolarity (osmoreceptors)
Cause of hyperglycaemic coma
inadequate blood flow to brain - severe salt and water depletion causing thirst and hypotension
Cause of hypoglycaemic coma
inadequate glucose to brain
Why is hyperglycaemia diabetes problem not self limiting?
liver still producing glucose
What is also transported with sodium and chloride in the loop of henle? importance?
potassium
loop diuretics can cause potassium wasting
How is energy supplied to the Na/K/Cl transport in ascending loop of henle?
Na/KATPase as the co-transporter is passive
