Sodium And Potassium Balance Flashcards
Which part of the brain is central to alter appetite for salt?
Lateral Parabrachial nucleus. This region takes information from other areas as well as from neurotransmitters including serotonin and glutamate and in euvolemia the main outcome is inhibition of sodium intake
Salt is often added to food to improve the flavour. Why does salt improve the flavour, but too much salt make food taste bad, and how do we sense this?
Salt is one of the 5 basic taste sensations, it is sensed by a specific sense of cells located on the tongue. At low salt concentrations the sensation is positive but as the concentration increases the sensation becomes aversive.
What proportion of filtered sodium load is taken up by
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule
Distal convoluted tubule
About 5%
Thick ascending limb of the loop of Henle
About 25%
Proximal convoluted tubule
About 65%
What proportion of renal blood flow is filtered into the nephrons
20%
What is the effect of increased tubular sodium concentration on the juxtaglomerular cells of the macular densa
Increased sodium uptake through the Na/K/Cl triple transporter, leading to release of adenosine and ATP
Which cells respond to the adenosine by reducing renin production
Extraglomerular mesangial cells
Why does the release of adenosine lead to a reduction in GFR in the short term
It causes the afferent SMCs to contract reducing renal plasma flow and therefore GFR
What is the effect of low tubular sodium at the macular densa on the production of Angiotensin II
It increases it because it stimulates the production of renin leading to angiotensinogen conversion to AI and finally to AII
Where in the tubular system does aldosterone work?
Distal DCT collecting duct
From where is aldosterone released?
Adrenal cortex
What is the effect of angiotensin2 on aldosterone release?
Increases it
how does aldosterone affect potassium balance?
Increases potassium secretion by stimulating sodium uptake: increased Na/K+ ATPase expression will increase the rate of K+ uptake and combined with the increase in Na reabsorption from the lumen (and excretion in to the blood) this will lead to increased K+ excretion
What is the effect og hypoaldosteronism on plasma renin?
It causes and increase in plasma renin because of the reduction in sodium reabsorption and the consequent loss of water reducing ECF and therefore BP. This leads to low sodium in the nephron and therefore the release of renin
What are the six major locations of baroreceptors?
Atria, right ventricle, pulmonary vasculature, carotid sinus, aortic arch, JGA
What are the effects of atrial natriuretic peptide (ANP) on sodium reabsorption in the PCT?
Reduces sodium reabsorption
What proportion of filtered potassium load is reabsorbed by:
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule
Distal convoluted tubule
Variable depending on potassium status ranges from 3% reabsorbed to secretion of 50%
Thick ascending limb of the loop of Henle
About 20%
Proximal convoluted tubule
About 65%
What happens to plasma potasssium after a meal?
Initially increases then taken up into cells by Na/K ATPase
Calculate the osmolarity of a solution containing 120mM NaCl, 5mM KCl, 10mM Na2HPO4, 5mM glucose at physiological pH
Na = (120 + 20) mM =140 mM
Cl = (120 +5) mM = 125 mM
K = 5 mM
HPO4 = 10mM
Glucose = 5mM
Total = 285mM of ‘particles’ = 285 mosmoles/L
A salmon swims from the sea into its home river. It is covered in small parasitic lice, why do the lice die?
The fish moves from a high salt to a low salt region. The sea lice are adapted to a high salt environment but are suddenly exposed to the low salt environment. Their cell membranes are semi-permeable and their extracellular and intracellular osmolarity is normally set to that of sea water. In the low salt environment, they take up water and their extracellular osmolarity drops. Now because their intracellular osmolarity is higher than the external osmolarity their cells take up water and swell. As they cannot regulate their osmolarity well, cell swelling leads to cell death and eventually to death of the parasite.
You are developing a new diuretic drug that targets a specific transporter protein
The effects of the drug in whole animals are as follows
Reduced renin production
Increased sodium excretion to 8% of filtered load
An early reduction in GFR that is prevented by co-treatment with furosemide
Which part of the nephron does this drug work in?
PCT
DCT
Thick Ascending limb of the Loop of Henle
Juxtaglomerular apparatus
Collecting duct
The drug acts in the PCT.
Diuretics work by increasing the osmolarity of the tubular fluid. Carbonic anhydrase inhibitors, mannitol, furosemide, are all diuretics that act in nephron segments prior to the juxtaglomerular apparatus. Which of these diuretics would lead to an early reduction in GFR by activating tubulo-glomerular feedback? Carbonic anhydrase inhibitors reduce PCT sodium reabsorption, mannitol is an osmotic diuretic as it is not reabsorbed and furosemide is a loop diuretic.
Mannitol and carbonic anhydrase inhibitors
Furosemide only
Carbonic anhydrase inhibitors and furosemide
Carbonic anhydrase inhibitors only
All three of them
Mannitol and carbonic anhydrase inhibitors
Tubuloglomerular feedback requires increased Na load in the distal nephron and a functional NKCCT2
All three give increased Na load (mannitol because it increases flow a bit like an increase in GFR) in the distal nephron. BUT furosemide does this by inhibiting NKCCT2 so this increase can’t be detected by the JGA
T or F: ICF volume varies with osmolarity?
F, ECF volume varies with osmolarity - it increases or decreases to maintain constant osmolarity
Which is the most prevalent and important solute in the ECF?
Sodium
What does Plasma sodium concentration have an effect on?
ECF volume, body weight, blood pressure
