US Lecture 6 - Sodium and Potassium Balance Flashcards
What is the main component of the ECF?
Sodium
What happens if you do a high sodium diet?
You will gain weight to try to balance the osmolarity but a decrease in sodium, reduces your weight
What are the effects of increasing sodium levels?
Increases osmolarity so the body increases ECF volume to reduce the osmolarity which causes an increase in blood volume and pressure
What are the effects of decreasing sodium levels?
Decreases osmolarity so the body decreases ECF to increase the osmolarity which causes a decrease in blood volume and pressure
Where is most sodium reabsorbed?
65% in the proximal convoluted tubule. 25% in ascending LoH, 8% in distal CT and 2% in CD
What happens if the GFR is increased/decreased to the reabsorption of sodium in the kidney?
As it is under relatively constant conditions, if GFR increases, so will Na reabsorption and vice versa
How is more Na reabsorbed from the body?
Reduce the amount of Na being filtered by -> reducing GFR
How is GFR reduced to reduce Na filtration into kidneys?
Arterioles (aff/efferent) are constricted - afferent more - which lowers the pressure so less filtrate goes through
What other ways of reabsorbing sodium is there?
The JGA stimulates the release of AngII, which acts of PCT to reabsorb more sodium. Also, aldosterone stimulates DCT and CT to reabsorb more Na If a low tubular Na is detected by the JGA, this stimmulates the release of AngII
How is sodium reabsorption decreased?
Atrial neturietic peptide -> dilates blood cells, reduces Na uptake in PCT/DCT/CD and reduces the stimulus on the JGA
What are the effects of sodium on the distal nephron?
Changes detected by JGA, which releases renin which stimulates cells in the liver to produce Ang > Ang I > Ang II
What stimulates and inhibits renin production?
Inhibits: increased BP and volume and decreased sympathetic stimulus Stimulates: decreased BP and volume and increased sympathetic stimulus
What are the effects of Ang II?
What is aldosterone?
Steroid hormone, synthesised and released from adrenal cortex in response to AngII, decrease in BP (baroreceptors) and decreased osmolarity of ultrafiltrate
What does aldosterone do?
Stimulates increased: Na reabsorption, K secretion and H+ secretion
What does excess aldosterone lead to?
Hypokalaemic alkalosis
How does aldosterone work?
Moves into cell and binds to a receptor inside the cell, inducing expression of apical Na channel of the collecting duct and promotes its activity. Also induces formation of Na-K-ATPase pumps
What are the diseases of aldosterone secretion?
Hypoaldosteronism, hyperaldosteronism and Liddle’s syndrome
What is hypoaldosteronism?
Reabsorption of sodium in the distal nephron reduced, increased urinary loss of sodium, ECF volume falls and increases renin, Ang II and ADH.
What are the symptoms of hypoaldosteronism?
Dizziness, low BP, salt craving and palpitations
What is hyperaldosteronism?
Reabsorption of Na at distal nephron is increased, reduced urinary loss of sodium, ECF volume increases, reduced renin, Ang II and ADH Increased ANP and BNP
What are the symptoms of hyperaldosteronism?
High BP, muscle weakness, polyuria, thirst
What is Liddle’s syndrome?
Inherited disease of high BP due to a mutation in the aldosterone activated Na channel, so channel is always ‘on’ -> leads to Na retention and hypertension
Where are baroreceptors present for the low pressure and high pressure side?
What are the responses to baroreceptor activity on the low pressure side?
What are the responses to baroreceptor activity on the high pressure side?
What is atrial natriuretic peptide?
Small peptide made in the atria which is released in response to atrial stretch
What does ANP do?
Vasodilation of renal blood vessels. Inhibition of Na reabsorption in PCT and CD. Inhibit release of renin and aldosterone. Reduces BP
What happens when there is an increase in ECF volume?
What happens when there is an decrease in ECF volume?
What are the different types of diuretic drugs?
Osmotic diuretics (glucose/mannitol), Carbonic anhydrase inhibitors, loop diuretics (furosemide, blocks triple co-transporter), thiazides (blocks Na/Cl cotransporter), K+ sparing diuretics (amiloride - blocks Na channels, spironolactone - aldosterone antagonist)
How do ACE inhibitors function to reduce Na reabsorption
Affect aldosterone levels and BP, reducing body’s ability to reabsorb Na directly and by increasing osmolarity of fluid going through
How do carbonic anhydrase inhibitors work?
Carbonic anhydrase helps to produce the H+, which are used in the transport of sodium, so sodium is not reabsorbed
How do loop diuretics work?
They block the triple transporters so sodium isn’t taken up into the lumen
How do thiazides work?
They block the Na/Cl cotransporter, leading to the intracellular Ca decreasing as the 3Na/Ca co-transporter becomes more active, so more calcium is reabsorbed from the filtrate
Where is potassium most abundant?
Intracellularly - 150mmol/l, with low extracellular conc - 3-5mmol/l
What are the effects of extracellular K+ on excitable membranes?
High conc: depolarises membranes > action potentials and heart arrhythmias Low conc: heart arrhythmias (asystole)
What happens to K+ after a meal?
K+ is absorbed, which increases plasma K+ and when stimulated by insulin (also by aldosterone and adrenaline) K+ is taken up by the tissues
What is the immediate response to dietary K+?
How much K+ is reabsorbed at LoH and distal convoluted tubule?
LoH - 30% DCT - 10%
How much K+ that was filtered ends up in the collecting duct?
Variable: 1-80% Variability depends on plasma [K+], aldosterone levels, tubular flow rate, plasma pH -> of which increasing these stimulates K+ secretion
How is potassium secreted by the principal cells?
Which channels does aldosterone stimulates for potassium transport?
What does flow do to K excretion and how?
Increases potassium excretion as prinicpal cells have primary cilia which when stimulated activate PDK1, which increases intracellular Ca increasing the activity of the Na/K pump
What is hypokalemia?
One of the most common electrolyte imbalances -> low potassium levels
What are the causes of hypokalemia?
Diuretics (due to increased tubular flow rates), surreptitious vomiting, diarrhoea, genetics -> Gitelman’s syndrome which is a mutation in Na/Cl transporter in the distal nephron
What is hyperkalemia?
Another common electrolyte imbalance -> too much potassium
What are some other causes of hyperkalemia?
Response to K+ sparing diuretics, ACE inhibitors and in the elderly
T OR F - when ADH/VP is high: 1) resulting urine is dilute 2) urine osmolarity is higher than osmolarity of blood 3) principal cells are permeable to water 4) renin secretion is increased 5) Aquaporins are relocated to the plasma membrane of the principal cells
1) F 2) T 3) T 4) F 5) T
In the LoH: (T/F) 1) ascending limb reabsorbs K+ 2) descending limb impermeable to water 3) Na+ reabsorption is required for uptake of glucose 4) Cells of descending limb have few microvilli 5) cells of ascending limb have many mitochondria
1) T 2) F 3) F 4) T 5) T
Regarding Na balance and regulation: (T/F) 1) Body sodium levels are used to regulate osmolarity 2) Under normal conditions increased GFR leads to increased Na reabsorption 3) Blocking the Na/Cl cotransporter in the DCT increases plasma Ca 4) Diuretics that inhibit aldosterone increase K+ secretion by increasing flow 5) Reduced Na in the DCT leads to renin secretion
1) F 2) T 3) T 4) F 5) T
What is absorbed in each of the sections of the nephron?
How is Na reabsorption increased or decreased in each part of the nephron?
