Lecture 5: Renal Hormones/Control of Body Water and Salt Flashcards

1
Q

Explain red blood cell production with low O2 delivery

A
  1. Low O2 delivery: hypoxia or ischemia
  2. Leads to an accumulation of hypoxia 1α (↑HIF-1α) in tubular interstitial cells
  3. This triggers the synthesis and release of Erythropoietin (Epoetin-α)
  4. Epoetin-α goes to bone barrow for RBC production (Erythroid Precursor Cells to normoblasts)

Review Slide 3

Erythropoietin comes from interstitial cells of kidney maturation of erythopoietycytes is controlled by Erythropoietin (Epoetin-α)

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2
Q

What is the difference between HIF-1α under normoxia and hypoxia?

A
  • In normoxia: HIF-1α is degraded
  • In hypoxia: active HIF dimer is produced and this leads to erythropoiesis (creation of RBC)
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3
Q

What does renin regulate?

A

blood pressure and sodium output

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4
Q

What is renin secreted by?

A

Juxtaglomerular cells (JG cells)

SMC has lots of renin

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5
Q

List the 3 mechanisms that trigger renin secretion?

A
  1. ↓ blood pressure activates renal vascular receptor (baroreceptor inside kidney) and ↑ renin release from JG cells
  2. ↓ blood pressure also ↓ GFR and delivery of Cl- to Macula Densa in the distal tubule which ↑ renin from JG cells
    3.↓ blood pressure causes a reflex activation of renal sympathetic nerves which ↑ renin release from JG cells.

all mechanisms are triggered by low BP

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6
Q

Is Angiotensin 2 a powerful vasodilator or constrictor?

A

Powerful vassoconstrictor, that’s why BP increases when it’s present

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7
Q

When BP decreases explain the effects of the Renin-Angiotension-Aldosterone System on factors listed below

  • Renin (kidney)
  • Angiotensin I
  • Angiotensin II
  • ADH & Thrist
  • FF
  • Aldosterone
  • Na+ Reabsorption
A
  • ↑ Renin (kidney)
  • ↑ Angiotensin I
  • ↑ Angiotensin II (vasoconstriction)
  • ↑ ADH & Thirst (water reabsorption)
  • ↑ FF (oncotic pressure)
  • ↑ Aldosterone
  • ↑ Na+ Reabsorption
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8
Q

Review Slide 10

A

Review Slide 10

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9
Q

How do renal prostaglandins respond to low blood pressure?

A

It responds to excessive vasoconstriction, so renal prostaglandins vasodilates

Review Slide 13

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10
Q

What two isoforms of prostaglandins are major renal Vasodilators?

A

PGE2 and PGI2 (in response to ↓ RBF)

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11
Q

What is Vioxx?

A

is a cyclooxygenase-2 (COX-2) inhibitor, and was recalled in 2004 because of increased risk of cardiovascular problems

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12
Q

What factors are the body trying to control in order to control body salt and water?

A

ECF volume and ECF osmolality

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13
Q

How can our body control water?

A

By controlling water intake and by controlling water output (intake=output)

Fluid: primary driver of intake, Urine: primary driver of output

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14
Q

Control of water intake is by thirst. What drives thirst? (4)

Stimuli of Thirst

A
  1. Increased Osmolality
  2. Decreased Arterial Pressure
  3. Decreased Blood Volume
  4. Angiotensin II

these all relate to ECF osmolality and ECF volume

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15
Q

How do we control water output?

A

By ADH secretion

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16
Q

What triggers ADH secretion? (7)

Stimuli of ADH secretion

A

1) Increased Osmolality
2) Decreased Arterial Pressure
3) Decreased Blood Volume
4) Angiotensin II
5) Trauma
6) Surgery
7) Drugs eg. opiates and anesthetics.

1-3 are all related to ECF osmolaloty and volume

17
Q

What occurs to Thirst and ADH secretion when there is an increase in plasma osmolality or decrease in BP?

A
  • Leads to an increase in thirst and increase in ADH secretion
  • Both leads to an increase in water retention in order to decrease plasma osmolality and increase BP
18
Q

Explain what is occuring in Area 1 and Area 2 in the image below

A
  • Area 1: Area b/w the two curves is sodium retention, Intake is increase but you are not excreting Na+ fast enough. The body is accumlating lots of Na+ and this leads to water reabsoprtion. Water reabsoprtion leads to weight gain
  • Area 2: Area b/w the two curves is sodium deficit. Intake is decreased but you are excreting Na+ too fast. The body has little Na+ and you are excreting more H2O. Excretion of H2O leads to weight loss.
19
Q

Regulation of Na+ Excretion

What occurs to the mechanisms listed below with an Increase in NaCl Intake

  • Blood Volume
  • Atrial Pressure
  • Arterial Pressure
  • Plasma Protein
  • ANP Secretion
  • GFR
  • Sympathetics
  • Renin
  • Angiotensin II
  • Aldosterone
  • Na+ Excretion

Either increases or decreases

HIGH yield

A
  • ↑ Blood Volume
  • ↑ Atrial Pressure
  • ↑ Arterial Pressure
  • ↓ Plasma Protein
  • ↑ ANP Secretion
  • ↑ GFR
  • ↓ Sympathetics
  • ↓ Renin
  • ↓ Angiotensin II
  • ↓ Aldosterone
  • ↑ Na+ Excretion (aka ↓ Na+ reabsorption)
20
Q

What occurs to the mechanisms listed below when Hemorrhage occurs

  • Blood Volume
  • Atrial Pressure
  • Arterial Pressure
  • ANP Secretion
  • GFR
  • Sympathetics
  • Renin
  • Angiotensin II
  • Aldosterone
  • ADH
  • H2O Excretion
  • Na+ Excretion

Either increases or decreases

HIGH yield
Hemorrhage-loss of blood

A
  • ↓ Blood Volume
  • ↓ Atrial Pressure
  • ↓ Arterial Pressure
  • ↓ ANP Secretion
  • ↓ GFR
  • ↑ Sympathetics
  • ↑ Renin
  • ↑ Angiotensin II
  • ↑ Aldosterone
  • ↑ ADH
  • ↓ H2O Excretion
  • ↓ Na+ Excretion (aka ↑ Na+ reabsorption)
21
Q

What does this D-Y graph shift represent?

A
  • Adrenal insufficiency
  • (cannot make enough aldosterone so you cannot reabsorb a lot of Na+-> you lose lots of Na+, hence ECF gets smaller)
22
Q

What does this D-Y graph shift represent?

A

SIADH (syndrome of inappropriate antidiuretic hormone-> lots of ADH so you keep reabsorbing water)

23
Q

What does this D-Y graph shift represent?

A

Infusion of isotonic NaCl ( Na+ and Cl- both go to the ECF compartment that is why it’s volume is raised)

24
Q

What does this D-Y graph shift represent?

A

High NaCl Intake