7 - Integrated Regulation of Sodium and Water Balance Flashcards

1
Q

What happens when sodium intake is increased from 30 to 300 mEq/day?

A

In a day or so after intake, excretion < intake, thus there is a positive sodium balance (retention).

The increased sodium is trapped in the ECF, leading to an increase in ECF osmolarity which leads to water retention to maintain osmolarity.

End result of sodium retention is no change in EC Na+ concentration with an expansion of ECFV.

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2
Q

The regulation of renal Na+ and it’s anions (Cl- and HCO3-) handling is important for the regulation of __________?

A

Extracellular fluid volume.

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3
Q

Why is sodium balance critical? What is the main way Na+ is regulated?

A

Body needs to maintain sufficient plasma volume to survive during low sodium intake, but must limit amount of sodium in body during excess sodium intake.

Regulated by excretion through adjusting GFR and reabsorption.

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4
Q

What are ways that GFR and/or reabsorption of Na can occur?

A

Endocrine, neural, paracrine, or autocrine changes.

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5
Q

Changes in sodium intake are sensed as changes in plasma volume. What are the three ways in which plasma volume changes are detected?

A
  1. Low pressure baroreceptors
  2. High pressure baroreceptors
  3. Intrarenal control via macula densa and renal vascular receptors.
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6
Q

Where are low pressure baroreceptors (volume receptors) found? What is the benefit of being in these locations?

A

Pulmonary veins and atria (low pressure circulation).

Venous side has high capacitance, so these sensors tend to respond first to changes in vascular volume.

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7
Q

How do low pressure baroreceptors in the pulmonary veins and atria respond to changes in volume? How much volume change is needed for a response to occur?

A

Decreased extracellular volume is sensed on the low pressure side of circulation, which results in increased renal sympathetic nerve activity.

These baroreceptors respond to 5-10% changes in volume.

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8
Q

Where are high pressure baroreceptors found?

A

Aortic arch and carotid sinus on the arterial (high pressure) side of circulation.

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9
Q

How do high pressure baroreceptors in the aortic arch and carotid sinus work?

A

Decreased pressure sensed on the high pressure side of circulation results in increased renal sympathetic nerve activity.

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10
Q

What is an intrarenal sensor of plasma volume? How does it work?

A

Renal afferent arteriole responds to altered stretch (change in intraluminal pressure) by altering the release of renin.

Decreased pressure in arteriole leads to increased renin released.

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11
Q

Describe the macula densa intrarenal sensor?

A

When there’s sustained decrease in extracellular volume and art pressure, GFR will fall and tubular reabsorption will be increased.

Results in decreased NaCl to nephron, including decreased NaCl to the macula densa
which causes increased release of renin.

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12
Q

How are the hormonal and neural systems involved in sodium balance?

A

Renin-angiotensin system

Aldosterone

Renal sympathetic nerves

Atrial natriuretic peptide

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13
Q

What is angiotensin?

A

An alpha-2-globulin released constitutively into the circulation by the liver.

By itself, it’s inactive.

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14
Q

Where is renin released from? What is its function?

A

Released from the granules on the afferent arteriole: cleaves angiotensin I (Ang1) from angiotensin.

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15
Q

What increases renin release?

A

Stimulation of the renal nerves, decreased afferent arteriole perfusion pressure, and decreased delivery of NaCl to the macula densa cells.

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16
Q

What is angiotensin II (AngII)? What cleaves it and where is the thing that cleaves it found?

A

Peptide formed when angiotensin converting enzyme (ACE) cleaves 2 aas from C-terminal of Ang1.

AVE found in epithelial cells and AngI is converted to AngII upon passaeg through the lungs.

17
Q

What is the function of AngII?

A

Potent vasocontrictor that increases systemic vascular resistance.

Alters renal function by constricting vasculature (thus decreases RBF and GFR) by increased PT reabsorption by stimulating the Na/H cotransport and stimulating the synthesis and release of aldosterone.

18
Q

Where is aldosterone synthesized and released? What is it’s release stimulated by?

A

cells in the zona glomerulosa in the adrenal gland.

Released stimulated by:

  1. Increased AngII
  2. Elevated plasma K+ concentration
19
Q

What is the function of aldosterone?

A

Directly stimulates Na+ reabsorption and K secretion in the principal cells of the DT and CCD.

20
Q

What are the fours ways in which a chronic elevation of aldosterone increases sodium reabsorption in the principal cells?

A
  1. Increase Na/K+ ATPase in basolateral membrane
  2. Increased expression of EnaC channels in the apical cell membrane
  3. Elevating serum glucocorticoid stimulated kinase levels (SGK1) which increases ENaC expression
  4. Stimulating CAP1 (channel activation protease-prostatin) which activates ENaC
21
Q

What is renal sympathetic nerve activity stimulated by?

A

Decreased ECF volume (low pressure baroreceptors) and decreased arterial pressure (high pressure baroreceptors).

22
Q

What are the three effects of renal nerve stimulation on renal function?

A
  1. Stimulate renin release
  2. Directly stimulate proximal tubular reabsorption (Na/H transporter)
  3. Vasocontrict renal vasculature - decreases GFR and RBF
23
Q

What causes release of atrial natriuretic peptide (ANP)? What are two ways that ANP alters renal function?

A

Increase volume/stretch of atria.

  1. Decreases sodium reabsorption in the CD
  2. Dilates renal vasculature to increase GFR
24
Q

What are physical ways to influence renal function? Give two examples

A

Alterations of hydrostatic and oncotic pressures.

Dilution of plasma protein (acute plasma volume expansion) causes an increased GFR by decreasing starling forces opposing filtration.

Dilution of plasma protein will decrease peritubular capillary reabsorption by decreasing cap oncotic pressure.

25
Q

What are three things that cause an increase in peritubular capillary pressure and thus a decrease in reabsorption?

A

Decreased afferent arteriole resistance

Decreased efferent arteriole resistance

Increased atrial pressure

26
Q

What are two things that cause an increase in peritubular colloid pressure and thus an increase in reabsorption?

A

Increase in systemic plasma colloid pressure and an increase in the glomerular filtration fraction.

27
Q

The kidney also plays a dominant role in regulating _______?

A

Blood volume and arterial blood pressure.

28
Q

Define feedback gain (equation)?

A

Correction in the original error divided by the remaining error.

Gain = correction/error

29
Q

What does it mean when it’s said that the level of arterial pressure “travels with the kidney”?

A

If a normotensive animal receives a kidney from a hypertensive donor, the recipient develops hypertension.

The reverse scenario is also true.

30
Q

What occurs when a renal artery is clamped? What conclusion can be drawn from this?

A

There’s an increase in systemic arterial pressure and renal perfusion pressure (distal renal arterial pressure).

This demonstrates the dominance of the kidney in long-term regulation of arterial blood pressure.

31
Q

What is one way that it’s hypothesized that the kidney serves as a master regulator of art pressure?

A

Through the pressure-natriuresis-diuresis mechanism.

32
Q

What is known about the pressure-netriuresis? When can this occur?

A

That increased renal perfusion pressure (RPP) increases sodium and water excretion in the absence of measurable changes in GFR and RBF.

This can also occur in the absence of any neural or hormonal input.

33
Q

What is pressure-induced natriuresis likely due to?

A

An alteration in renal tubular transport

There is a significant reduction in fractional sodium reabsorption as renal perfusion pressure (RPP) is increased.

34
Q

What is thought to inhibit PT transport of sodium?

A

Internalization of transporters, ie the movement of Na/H exchanger from apical membrane to vesicles in the cytoplasm.