6. Sodium and Potassium Balance

Question 1

Because humans maintain a constant osmolarity what happens when the salt increases?

Answer 1

Water also increases, increasing the volume

Question 2

Describe the relationship between number of mosmoles in the ECF and the volume of the ECF?

Answer 2

The number of mosmoles in ECF is proportional to the volume of ECF

Question 3

What is the main determinant of ECF volume?

Answer 3

Sodium because it is the main solute

Question 4

What is the effect of a high salt diet?

Answer 4

Increase body weight

Question 5

What effect does increases sodium have?

Answer 5

Increased osmolarity -> increased ECF volume -> increases blood volume and pressure
Viceversa

Question 6

How much sodium is reabsorbed in the PCT?

Answer 6

65%

Question 7

How much sodium is reabsorbed in the ascending limb?

Answer 7

~25%

Question 8

How much sodium is reabsorbed in the DCT?

Answer 8

8%

Question 9

How much sodium is reabsorbed in the collecting dect?

Answer 9

2%

Question 10

If you increase the GFR what else is increased?

Answer 10

The amount of sodium reabsorbed also increases

Question 11

If you decrease the GFR what else decreases?

Answer 11

The amount of sodium reabsorbed decreases

Question 12

What is the principle for retaining more sodium?

Answer 12

Reduce the amount of sodium going into the tubular system

Question 13

How can you prevent more sodium from entering the tubular system?

Answer 13

Increases sympathetic activity - restricting arteriole = reducing blood flow and the perfusion pressure gradient, Also stimulates the PCT to remove more Na, Also activation of cells in the JGA leading to the production of Angiotensin II.
Angiotensin II - affects the PCT in the same way, stimulates the production of aldosterone
Aldosterone - causes the increased Na+ uptake in the DCT and CT

Question 14

What does Atrial Naturietic peptide do?

Answer 14

It decreases Na reabsorbtion

Question 15

What is the effect of reduced sodium in the juxtaglomerular apparatus?

Answer 15

The macula densa shrink, and release prostaglandin II stimulating the juxtaglomerular cells to produce renin.

Question 16

Where is renin produced?

Answer 16

In the JGC of kidney

Question 17

Where is angiotensinogen produced

Answer 17

Liver

Question 18

What gives the release of renin?

Answer 18

Reduced BP and fluid volume

Question 19

What is the effect of angiotenin II?

Answer 19

Increases Na+ uptake in the PCT –> increased BP
Causes constriction of the vascular system –> increased BP
Goes too the adrenal glands (cortex) to synthesis aldosterone synthesis

Question 20

What type of hormone is aldosterone?

Answer 20

Steroid hormone

Question 21

Where is aldosterone synthesised?

Answer 21

In the adrenal cortex

Question 22

What stimulates the release of aldosterone?

Answer 22

decrease in BP via baroreceptors, decrease osmolarity of ultrafiltrate

Question 23

What does aldosterone stimulate?

Answer 23

Increases sodium absorption
Potassium secretion
Hydrogen secretion

Question 24

What does an excess of aldosterone cause?

Answer 24

Hypokalaemic alkalosis

Question 25

How does aldosterone increase sodium reabsorbtion?

Answer 25

It increases Na+/K+ATPase and the transporter in the lumen membrane

Question 26

What is hypoaldosteronism?

Answer 26

1) Causes reduced sodium reabsorption in distal nephron 2) Increases the urinary loss of sodium 3) ECF volume falls 4) Increased renin, Ang II and ADH

Question 27

What effect does fall in ECF volume and increased renin, Ang II and ADH have?

Answer 27

Dissiness Low BP Salt craving Palpitation

Question 28

What region of nephron does aldosterone affect?

Answer 28

collecting duct, Distal DCT

Question 29

What is hyperaldosteronism?

Answer 29

1) Increased reabsorption in the distal nephron 2) decreases urinary loss of Na+ 3) The ECF volume increases 4) Reduced renin, ANg II and ADH 5) Increased ANP and BNP

Question 30

What effect does hyperaldosteronism have on the body?

Answer 30

High BP Muscle weakness Polyuria Thirst

Question 31

Describe Liddle's Syndrome?

Answer 31

This is where the channels don't respond to the aldosterone activated sodium channel. So the channel is always on resulting in sodium retention and ultimately hypertension

Question 32

What is the response of low pressure on baroreceptors on the low pressure side?

Answer 32

Signal through afferent fibres to brain stem --> sympathetic activity --> ADH release

Question 33

What is the response of high pressure on baroreceptors on the low pressure side?

Answer 33

Atrial stretch --> ANP, BNP released

Question 34

What is the response of low pressure on baroreceptors on the high pressure side?

Answer 34

Signals through afferent fibres to the brainstem --> sympathetic activity --> ADH release JGA cells --> renin release

Question 35

What is the action of ANP?

Answer 35

Vasodilation of renal and other systemic blood vessels Inhibition of Na+ reabsorption in proximal tubule and in the collecting ducts Inhibits the release of renin and aldosterone Reduces blood pressure

Question 36

How do diuretics work?

Answer 36

By reducing the levels of Na+ reabsorbed in the tubular fluid it will increase in the osmolarity of the tubular fluid. It will decrease the diffusion gradient for water so more fluid will be lost. Overall effect reduction in BP

Question 37

What is the effect of ACE inhibitors?

Answer 37

Reduce the vasoconstriction effect caused by Ang II | Because there is reduced Ang II you also block sodium uptake

Question 38

List diuretic drugs

Answer 38

Osmotic diuretics (glucose) Carbonic anyhydrase inhibitors Loop diuretics (Blocks triple transporter - furosemide) Thiazides (block Na/Cl cotransporter) DCT K+ sparring diuretics

Question 39

Give two K+ sparring diuretics?

Answer 39

Amiloride - block Na channels | Spironolactone - aldosterone antagonist

Question 40

How do carbonic anhydrase inhibitors work?

Answer 40

By blocking carbonic anhydrase essentially H2CO3 cannot be brought into the cell and dissociate into HCO3- and H+. Without H+ a transporter cannot exchange the H+ with an Na+. Increases tubular concentrations of Na+

Question 41

What is the intracellular concentration of K+?

Answer 41

150mmol/L

Question 42

What effect does extracellular K+ have on excitable membranes (nerve and muscle)

Answer 42

High K+ ; depolarises the membranes - action potentials, arrhythmias Low K+ ; heart arrhythmias (asystole)

Question 43

What stimulates K+ uptake into cells?

Answer 43

Insulin (aldosterone and Adrenalin)

Question 44

How much potassium is absorbed in the PCT?

Answer 44

60-70%

Question 45

How much potassium reaches the distal convoluted tubule?

Answer 45

10%

Question 46

What causes the secretion of K+?

Answer 46

High: plasma [K+], aldosterone, tubular flow rate and plasma pH

Question 47

What cells actively transports K+ into cells from the blood, where they can diffuse through channels into the tubule?

Answer 47

Principle cells

Question 48

How does aldosterone increase K+ secretion?

Answer 48

Increases Na+ intake, more sodium is pumped out on the basolateral membrane so more potassium is brought in. Then if more potassium comes in more potassium can diffuse out into the tubule

Question 49

How does tubular flow rate increase K+ secretion?

Answer 49

Principle cells have cilia which when there is an increase flow rate the cilia activate PDK1. PDK1 releases Ca2+ which increases the activity of a K+ channel

Question 50

What is hypokalemia?

Answer 50

Low potassium concentration

Question 51

What situations is hypokalemia often seen?

Answer 51

Diuretics Surreptitious vomiting Diarrhoea Genetics (Gitelman's syndrome; mutation in Na/Cl transporter in distal nephron) Seen in response to K+ sparring diuretics ACE inhibitor patients Elderly