Sodium and Potassium - part of Tubular Function - have been through. Flashcards

1
Q

What happens to ECF volume if you have prolonged high sodium diet?

A

Retain more water, and therefore gain weight (you gain water to keep osmolarity constant). This leads to increased blood pressure, and blood volume. The opposite happens for decreased dietary sodium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

State the relative amounts of sodium reabsorbed in different parts of the nephron.

A

65% - PCT 25% - loop of Henle 8% - DCT Up to 2% - collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the relationship between GFR and sodium reabsorption.

A

The greater the GFR the greater the sodium reabsorption, but proportions remain the same.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is Na+ reabsorption increased in the nephron and Na+ levels preserved? (x5 components of the mechanism)

A
  1. LOW BLOOD PRESSURE increases sodium reabsorption by REDUCING GFR; so more Na+ retained in blood rather than entering filtrate which increases water retention.
  2. Low GFR also promoted by SNS activity - which causes vasoconstriction of afferent arteriole, so less blood reaches the nephron.
  3. Another effect of increased SNS means PCT reabsorbs more sodium.
  4. SNS activity activates juxtaglomerular apparatus –> grannular cells secrete renin which increases Angiotensin II. Angiotensin II (increases blood pressure by vasoconstriction and) stimulates uptake of Na+ in PCT.
  5. Angiotensin II also increases aldosterone levels which affects DCT and collecting duct by increasing Na+ uptake.
  6. Low tubular sodium at juxtaglomerular apparatus also increases production of renin which increases angiotensin II and aldosterone – to mediate the same effects described above.

——-> Overall effect = raised BP (because sodium reabsorption results in passive flow of water to balance osmolarity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What triggers the juxtaglomerular apparatus to produce renin? (x3)

A

Low tubular Na+ concentration Low renal perfusion pressure. SNS activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What hormone is involved in decreasing sodium reabsorption? What is the mechanism? (x4 components)

A

Atrial naturietic peptide increases GFR by by (i) increases diameter of afferent (and systemic blood vessels), and constricts efferent arteriole; (ii) reduces PCT activity; (iii) suppresses renin release at juxta apparatus; (iv) reduces Na+ reabsorption in collecting tubules esp. thick ascending limb.

OVERALL AIM IS TO REDUCE BLOOD PRESSURE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe process of renin release? Triggers? (x3)

A

Activity of Na+/K+/Cl- channel in DCT senses amount of salt in the system at macula densa.

–> If there’s not much salt, amount of sodium going into tubule cells falls. Therefore, cells have a low osmolarity compared to the envoiroment they’re sat in, so water moves out into interstitium. They therefore shrink, and thus produce PGe2 and NO, stimulates release of renin from glomerular cells.

—> (As well as low osmolarity) ALSO STIMUALTED BY SNS AND HORMONES.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where do you find a lot of ACE? REMINDER - what is the function of ACE?

A

Lung Endothelium. REMINDER: ACE converts Angiotensin I to Angiotensin II.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What effect does angiotensin II have? (x3) In each case, where does it effect?

A

(1) Increase sodium reabsorption in the PCT. Subsequently increases water reabsorption = increased BP.
(2) Vasoconstriction –> also increases BP.
(3) Increases aldosterone synthesis in adrenal glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

To stimulate Na absorption, what 3 stimuli?

A

decrease blood pressure, decrease fluid volume, increase sympathetic stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the effects of aldosterone on absorption and secretion. (x3)

A

Increase Na+ reabsorption, Increases H+ secretion, Increases K+ secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the result of aldosterone excess?

A

Hypokalemic Alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which cells does aldosterone work on

A

Principal cells in the collecting duct (and DCT).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does aldosterone work? How does it cause an increase in sodium reabsorption? (x3 effects)

A

Aldosterone is a steroid so it has a genomic effect.

–> binds to steroid hormone receptor in cytoplasm (type 1 intracellular receptors).

—> It relocalises the vesicles containing sodium transporters to the apical membrane.

–> It also increases transcription and production of more sodium channels and Na+/K+ ATPase on basolateral membrane and Na+ channels on apical membrane.

–> increase expression of regulatory proteins which open the Na+ channels on the apical membrane.

RESULT: increase sodium reabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the consequences of hypoaldosteronism?

A

(1) Reabsorption of sodium in the distal nephron is reduced (2) Increased urinary loss of sodium (3) ECF volume falls (4) Increased renin and Angiotensin II and Vasopressin secretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the symptoms of hypoaldosteronism?

A

Low blood pressure, dizziness, palpitations, salt craving.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the consequences of hyperaldosteronism?

A

(1) Increased sodium reabsorption in the distal nephron. (2) Reduced urinary loss of sodium (3) ECF volume increases - HYPERTENSION (4) Reduced angiotensin and vasopressin secretion (5) Increased ANP and BNP (niuretic peptide).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Liddle’s Syndrome?

A

Mutation in the aldosterone dependent Na+ channel - the channel is permanently switched on resulting in sodium retention from constant sodium reabsorption; which leads to HYPERTENSION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms of hyperalldosteronism?

A

High blood pressire, muscle weakness, polyuria and thirst.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does low pressure stimulate?

A

RAS - more angiotensin II produced Increase sympathetic activity Increase ADH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is ANP produced and what does it do?

A

ANP is produced by atrial stretch It causes vasodilation of renal blood vessels Inhibition of sodium absorption in the PCT and in collecting ducts Inhibits release of renin and aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the two locations of baroreceptor?

A

Heart and vascular system.

23
Q

Which of the baroreceptors in the body are exposed to low pressure and high pressure? How is this presure defined?

A

LOW PRESSURE: before the left ventricle. HIGH PRESSURE: after left ventricle.

24
Q

How do baroreceptors on low pressure side respond to change in pressure?

A

CAN RESPONDS TO LOW AND HIGH PRESSURE! (1) decrease in pressure –> signal to brainstem which increases sympathetic activity and ADH secretion. (2) increase in pressure –> Atrial stretch which causes release of ANP and BNP.

25
Q

How do baroreceptors on high pressure side respond to change in pressure? (x2 mechanisms)

A

ONLY RESPOND TO LOW BLOOD PRESSURE: decrease in pressure signal through afferent brain fibres to brainstem which increases SNA and ADH secretion. AND signals from JGA, causes renin release.

26
Q

How can GFR be affected to help lose sodium?

A

Increase GFR = more sodium removed.

27
Q

Describe the effects of ACE inhibitors on sodium reabsorption. (direct and indirect effect)

A

(DIRECT) ACE inhibitors reduce the amount of sodium reabsorption in the PCT and inhibit vasoconstriction (caused by drop in Angiotensin II). (INDIRECT) And they reduce the amount of sodium reabsorption in the DCT and collecting duct (due to indirect inhibition of aldosterone production). OVERALL AIM: LOWER BLOOD PRESSURE.

28
Q

State five types of diuretics and where they act in the nephron.

A

Osmotic diuretics (glucose is an osmotic diuretic in diabetics, and mannitol)

Carbonic Anhydrase Inhibitors (in PCT cells)

Loop Diuretics

Thiazide Diuretics (DCT cells)

Potassium Sparing Diuretics (distal part of nephron - DCT and cortical collecting duct).

29
Q

What is the basis behind diuretics with regards to tubular osmolarity?

A

They increase the tubular fluid osmolarity so there is less of a gradient between the collecting duct and the interstitial compartment so less water is reabsorbed.

30
Q

How do carbonic anhydrase inhibiotrs work?

A

Carbonic anhydrase important in HCO3- reabsorption and exportion of H+ at the expense of Na+. Therefore, if carbonic anhydrase inhibited, H+ production inhibited in PCT cells; if there’s less H+ for export, then less Na+ can come in, so less Na+ reabsorbed and so more Na+ reaches distal part of nephron – which means less water reabsorbed in distal nephron region.

31
Q

What do loop diuretics do? Name a loop diuretic.

A

Furosemide - they block the Na+/K+/Cl- triple transporter

32
Q

What are the most potent diuretics and why?

A

Loop diuretics. Because they stop reaborpsion of salt (so tubular fluid has higher osmolarity when it reaches collecting duct) AND they prevent salt accumulation in medullary interstitium.

33
Q

What do thiazide diuretics do?

A

Inhibit Na+/Cl- cotransporter

34
Q

What do K+ sparing diuretics do? Name two.

A

Amiloride - Na+ channel blocker - prevents entry of Na+ from the tubule lumen. Spironolactone - aldosterone antagonist

35
Q

Why do you get a smaller natriuresis with K+ sparing diuretics?

A

Because they act on the distal region of the nephron, which is only responsible for 2% of the reabsorption of Na+

36
Q

Why are they called K+ sparing diuretics?

A

They don’t cause increased excretion of K+

37
Q

What is a consequence of high extracellular K+?

A

It can cause depolarisation of membranes (e.g. resulting in arrhythmia)

38
Q

What is the effect of low extracellular K+?

A

Heart arrhythmias also (asystole).

39
Q

What happens to plasma potassium? What stimulates this? (x3) Why is it taken up so quickly?

A

Taken up into tissues, so extracellular levels remain low, but INSULIN Aldosterone and Adrenaline.

Taken up so quickly because of the Na+/K+ pump found across almost all cells across the body.

40
Q

What is the fraction of filtered K+ reachng different points in the nephron?

A

30% in picture means 70% absorbed in PCT.

41
Q

What stimulates K+ secretion? (x4)

A

Increase in plasma K+ concentration, Aldosterone increase, Increase in tubular flow rate and Increase in pH.

42
Q

What is the mechanism of K+ secretion and where does it occur?

A

Potassium secreted by principal cells of collecing ducts.
Na+/K+ ATPase pumps K+ into ductule cells, and move out pasively by apical membrane channels.
Also regulated by membrane electric potential because K is positive.

43
Q

How does aldosterone stimulate K+ secretion?

A

Stimulates both ATPase and apical channel.

44
Q

How does tubular flow affect K+ secretion? Mechanism?

A

TUBULAR FLOW STIMUALTES POTASSIUM EXCRETION AND therefore STIMULATES SECRETION.

  1. Principal cells have cilia that move with the flow.
  2. As flow increases, the movement of the cilium stimulates a protein called PDK1, which stimulates an increase in intracellular Ca2+ concentration.
  3. This stimulates the activity of the K+ channels.
45
Q

What is the effect of diuretics on K+ secretion?

A

Flow is increased by diuretics, which is one of the problems with non-potassium sparing diuretics because they cause an increase in K+ secretion

46
Q

State some causes of hypokalaemia. (x4)

A

Diuretics, Diarrhoea, Surreptitious Vomiting, mutations in transporters

47
Q

State some causes of hyperkalaemia. (x3)

A

Ageing, Potassium-sparing diuretics, ACE inhibitors

48
Q

What is intracellular K+ concn

A

150 mmol

49
Q

Does the ascending loop absorb K+

A

yes

50
Q

Do the descending limb cells have few microvilli?

A

Yes

51
Q

does blocking na/cl cannnel increase calcium?

A

yes

52
Q

What triggers ANP release?

A

Repsonse to atrial stretch from increased blood pressure – remember, ANP reduces blood pressure.

53
Q

Where is ANP produced? What else is produced with it?

A

Produced in atria with BNP.