ECF Volume Regulation 1

Question 1

Is H20 able to pass through all membranes?

Answer 1

Yes

Question 2

What are the major ECF osmoles?

Answer 2

Na+ and Cl+

Question 3

What are major ICF osmoles?

Answer 3

K+ salts

Question 4

What is always the affect of a change in ECF Na+ levels?

Answer 4

A change in ECF volume

Question 5

What receptors is the regulation of Na+ dependent on?

Answer 5

High and low P baroreceptors

Question 6

What is an abnormally low ECF volume known as?

Answer 6

Hypovolaemia

Question 7

Describe the renal response to salt and water loss as a result of vomiting, diarrhoea or excess sweating

Answer 7

There is decreased blood volume which results in decreased venous pressure and decreased venous return. There is therefore reduced atrial pressure and decreases EDV, therefore reduced SV, CO and BP

Sympathetic discharge increases VC which increases TPR and BP towards normal

Question 8

What happens in terms of receptors and nervous innervation when a drop in BP and BV is detected?

Answer 8

The carotid sinus baroreceptors recognise the drop and their inhibition of sympathetic discharge decreases. The resulting increased sympathetic discharge results in vasoconstriction and increased TPR and therefore increases the BP back towards normal pressure

Question 9

What prompts increased ADH release in situations of water and salt loss?

Answer 9

Reduced atrial pressure detected by the atrial baroreceptors and carotid sinus baroreceptor inhibition

Question 10

What are the effects in the kidney when carotid sinus baroreceptor inhibition of sympathetic innervation decreases in response to low BP?

Answer 10

VC, TPR and BP increase, the the kidney undergoes increased arterial constriction and therefore less Na is passing via the JG cells, which therefore produce renin, and thus Angiotensin II

Question 11

What are the affects of renin production in the kidney?

Answer 11

This is converted to Angiotensin II which causes increased proximal tubule reabsorption of NaCl and H20 to increase water retention, and also stimulates aldosterone release from the adrenal cortex which increased the distal tubule reabsorption of NaCl and H20

Question 12

What prompts the release of renin from the kidney in terms of sympathetic innervation?

Answer 12

The systemic sympathetic innervation causes vasoconstriction, including of the afferent arteriole, reducing the flow pass the JG cells of Na, which detect this and produce renin to increase reabsorption

Question 13

How does angiotensin II increase reabsorption from the tubule? (proximal)

Answer 13

By decreasing the peritubular capillary hydrostatic pressure (creates high to low from tubule to capillary)

Question 14

What determines the changes in rate of uptake from the tubule to the peritubular capillaries?

Answer 14

The plasma protein concentration

Question 15

What percentage of NaCl and H20 is reabsorbed at the proximal tubule in low BP situations/hypovolaemia?

Answer 15

65%

Question 16

What percentage of NaCl and H20 is reabsorbed at the proximal tubule in situations of high BP/hypervolaemia?

Answer 16

75%

Question 17

Is the GFR significantly affected by the portion of NaCl and H20 reabsorbed at the proximal tubule?

Answer 17

No, unless the volume depletion is severe enough to cause considerably lowered MBP

Question 18

What system maintains the GFR unless in severe fluid depletion?

Answer 18

The constriction of the afferent arteriole by sympathetic innervation balanced by the Angiotensin II mediated constriction of the efferent arteriole

Question 19

What controls the distal tubule Na reabsorption?

Answer 19

Aldosterone

Question 20

How does the kidney ultimately control aldosterone secretion?

Answer 20

Via the Juxtaglomerular apparatus. Cells in a specialised loop of the distal tubule as it passes the afferent arteriole, known as the macula densa. The juxtaglomerular cells combined with the macula dense form the juxtaglomerular apparatus. These function by detecting the amount of Na passing by the cells in the afferent arteriole and when the Na(Cl) levels are low, the JG apparatus secretes renin, as well as detecting a drop in the blood pressure in the afferent arteriole, which has the same effect of renin production. The renin is ultimately converted to Angiotensin II in the plasma and one of the effects of it is to stimulate the adrenal cortex to produce aldosterone, increasing the reabsorption at the distal tubule

Question 21

What is the only regulated step in the Angiotensin pathways?

Answer 21

The production of renin as result of a drop in blood pressure

Question 22

What is the enzyme which converts angiotensin I to angiotensin II?

Answer 22

Angiotensin Converting Enzyme (ACE)

Question 23

What step in the angiotensin pathway is the rate limiting step? Why?

Answer 23

The renin release
Angiotensin is always in the plasma, it only exerts its effects when converted to Angiotensin I (and onwards) in the plasma by the renin

Question 24

What controls the renal baroreceptors (JG cells) ability to secretion renin when distended?

Answer 24

Nothing, it is an intrinsic property that occurs even if denervated

Question 25

What factors cause renin release (3 things)?

Answer 25

1. The JG cells detecting a drop in pressure in the afferent arteriole
2. Sympathetic nerve activity causes renin release via Beta1 effects
3. The rate of renin secretion is inversely proportionate to the Na(Cl) passing at the macula densa

Question 26

How is renin release inhibited (2 ways)?

Answer 26

1. Angiotensin II feeds back eventually to inhibit renin

2. ADH inhibits renin release via osmotic control

Question 27

Describe the vasoconstrictive properties of Angiotensin II

Answer 27

It is an extremely potent vasoconstrictor, between 5 and 10 times more potent than norepinephrine and therefore contributes to increased TPR in hypovolaemia

Question 28

What are the function of Angiotensin II? (4 things)

Answer 28

1. Stimulates aldosterone and NaCl and H20 retention
2. It is a very potent biological vasoconstrictor, many times more effective than noradrenaline and therefore contributes to an increase in TPR and BP
3. It acts on the hypothalamus to stimulate ADH secretion and therefore H20 reabsorption from the CD
4. It stimulates the thirst mechanisms and salt appetite in the hypothalamus

Question 29

Describe the response of the kidney to increased GFR

Answer 29

GFR increases
Flow through the tubule increases
Flow past the macula dense increases
Paracrine from macular densa to afferent arteriole
Afferent arteriole constricts
Resistance in afferent arteriole increases
Hydrostatic pressure in glomerulus decreases
GFR decreases

Question 30

What is the response of the kidneys in a scenario where a person who is suffering from severe diarrhoea has lost 3l of salt and water, and then drunk 2l pure water?

Answer 30

There opposing inputs to ADH secreting cells:

The ECF osmolarity has decreased (more water less salt) and this results in inhibition of ADH via osmoreceptors
BUT
ECF volume has decreased so the ADH is increased via the baroreceptors

Question 31

What can be said about the volume considerations vs the osmolarity considerations regarding the ECF when there is a change in both in the kidney? What is the purpose of this?

Answer 31

Normally, when the volume if within the usual range, the osmolarity is the main determinant of ADH. However, if there is sufficient change to compromise brain perfusion, the volume change always has priority and the change in osmolarity can be worsened as a result but the body will always work to sustain EFC volume regardless
This emergency mechanism saves perfusion for the brain as ultimately extreme hypovolaemia is not sustainable for the brain

Question 32

What is important to note when giving fluid resuscitation in patients with severe fluid loss? Why?

Answer 32

You MUST NOT give pure water to a patient with fluid loss, but instead saline infusion

They have lost large amounts of salt along with the water they have lost, so the replacement fluids must maintain the normal balance of tonicity