Renal Physl 14 Flashcards

1
Q

What does excess sodium do?

A
  • Increases plasma osmolarity
  • Drives renal water absorption and thirst
  • Expansion of blood volume which increases BP
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2
Q

What happens when excess salt is ingested?

A

There is an increase in osmolarity causing vasopressin to be released (which increases reabsorption of water). Thirst mechanisms also increase water intake so more water is available for reabsorption

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3
Q

What happens when there is an increase of extracellular fluid volume?

A

The kidneys will increase their excretion of salt and water

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4
Q

What is the difference in timing of the kidneys lowering an increase in extracellular fluid volume vs cardiovascular reflexes?

A

The kidneys are quite slow while cardiovascular reflexes can lower blood pressure on the order to seconds to minutes

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5
Q

What does plasma osmolarity return to normal as a result of?

A

As a result of water intake and the adjustments by the kidneys and cardiovascular system

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6
Q

What is sodium balance significantly influenced by?

A

Hormonal controls

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7
Q

Where is Aldosterone synthesized?

A

At the adrenal cortex

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8
Q

Which part of the nephron does aldosterone work at?

A

At principal cells of the renal distal tubule and the collecting duct

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9
Q

What reabsorption does Aldosterone stimulate?

A

Sodium reabsorption

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10
Q

How does Aldosterone increase sodium reabsorption?

A

By increasing activity of the basolateral Na-K-ATPase

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11
Q

What happens as a result of aldosterone stimulating the basolateral Na-K-ATPase?

A

Sodium is reabsorbed and potassium is excreted

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12
Q

What is the mechanism of aldosterone?

A

It circulates in the blood to act at the kidneys by diffusing into principal cells and binds to a cytoplasmic receptor which stimulates transcription and translation and protein synthesis which results in Na-K-ATPase pumps on the basolateral membrane and also modulates them to speed up their action

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13
Q

What is the end result of aldosterone?

A

There is increased sodium reabsorption and potassium excretion which increases blood pressure

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14
Q

What stimulates Aldosterone release?

A

Low blood volume/pressure and high circulating potassium

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15
Q

What cascade does low BP trigger?

A

The renin angiotensin aldosterone cascade

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16
Q

What does Angiotensin II stimulate the adrenal cortex to produce?

A

Aldosterone

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17
Q

How can high plasma osmolarity affect aldosterone production?

A

It suppresses aldosterone production to prevent salt from being reabsorbed

18
Q

What does a large decrease in plasma osmolarity do to aldosterone?

A

It stimulates aldosterone secretion which helps to reabsorb sodium

19
Q

How does the arterial baroreflex affect the renal sympathetic nerve activity in response to low BP?

A

It increases renal sympathetic nerve activity

20
Q

What does increased renal nerve sympathetic activity do to the juxtaglomerular cells in the kidney?

A

Cause it to secrete renin

21
Q

What does Renin do?

A

Converts angiotensinogen to angiotensin I

22
Q

What does ACE do?

A

Converts Angiotensin I to Angiotensin II

23
Q

What does angiotensin II do?

A

Acts on the adrenal cortex to stimulate aldosterone release

24
Q

What does aldosterone release do?

A

Stimulates sodium reabsorption and potassium excretion

25
Q

What does an increased sodium reabsorption caused by aldosteronedo?

A
  • Increases plasma osmolarity which stimulates thirst and water intakes
  • Stimulates water reabsorption
26
Q

How can angiotensin II affect the brain?

A

It stimulates vasopressin release by the hypothalamus

27
Q

What does vasopressin released by the hypothalamus do?

A

Increases renal water absorption and helps restore blood volume and pressure

28
Q

How does angiotensin II affect the vasculature?

A

It causes Vasoconstriction which increases BP

29
Q

How does angiotensin II affect sympathetic outflow at the brain?

A

It causes an increase in sympathetic output which increases cardiac output and an increase vasoconstriction and further stimulates the RAAS cascade

30
Q

How does angiotensin II act at the proximal tubule?

A

It stimulates the apical Na-H-exchanger which stimulates salt and water reabsorption

31
Q

What is the overall effect of the RAAS system?

A

It increases blood volume and pressure

32
Q

What is salt apetitie?

A

A powerful craving for salty foods when plasma osmolarity drops

33
Q

What hormones is salt appetite linked to?

A

The presence of angiotensin II and aldosterone

34
Q

What do Atrial Natriuretic Peptides do?

A

Increase sodium excretion in the urine

35
Q

What are Natriuretic Peptides released by?

A

Myocardial cells

36
Q

What is atrial Natriuretic Peptides synthesized by?

A

The cardiac atria

37
Q

When is ANP typically released?

A

In conditions of increased blood volume and pressure

38
Q

What in brain natriuretic peptide release by?

A

Ventricular myocardium

39
Q

What induces the release of Natriuretic Peptides?

A

High volume condition that cause cardiac muscle to be stretched

40
Q

How does ANP act on the kidneys?

A

It induces sodium and water excretion which helps restore blood volume and pressure back down to normal by dilating the afferent arteriole and inhibiting sodium reabsorption in the collecting duct. Also inhibits the release of sodium/water reabsorbing mediatiors