Renal Physiology Lecture 2: Sodium Balance Flashcards

1
Q

What happens in kidneys with excess sodium?

A
  • increases plasma osmolarity
  • drives renal water reabsorption & thirst
  • Expansion of blood volume due to retention of water
    • increases arterial pressure
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2
Q

Mechanism of salt ingestion

A
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3
Q

What hormone control sodium balance

A

Aldosterone

  • Synthesized in the adrenal cortex → circulates in the blood
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4
Q

Where does aldosterone act?

A

at the renal distal tubule and collecting duct

  • At principle cells
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5
Q

Function of Aldosterone

A
  • Stimulates sodium reabsorption
  • Increases acitvity of Na-K-ATPase
  • Increases potassium excretion
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6
Q

Aldosterone process

A
  • Aldosterone combines with a cytoplasmic receptor
  • Hormone-receptor complex intiates trnascription in the nucleus
  • Translation and protein synthesis makes new protein channels and pumps
  • Aldosterone-induced proteins moldultes existing channels and pumps
  • Result is increases Na reabsorption and K secretion
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7
Q

What stimulates aldosterone release?

A

Plasma osmolarity & blood volume/ pressure

  • Low blood volume/ pressure, high circulating potassium stimulates aldosterone release
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8
Q

How does potassium stimulate aldosterone release?

A

High potassium acts directly at the adrenal cortex

  • Aldosterone results in increased potassium excretion, protecting from high potassium levels
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9
Q

Effect of osmolarity & blood pressure/ volume on aldosterone release

A
  • Low pressure/ volume initiates mechanisms for salt/ water reabsorption by kidneys and production of Angiotensin II (Ang II) and aldosterone
  • High plasma osmolarity (dehydration) suppresses aldosterone production
  • decreased plasma osmolarity stimulates aldosterone production
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10
Q

RAAS

A

Renin-Angiotensin-Aldosterone System

  • a hormone system within the body that is essential for the regulation of blood pressure and fluid balance. The system is mainly comprised of the three hormones renin, angiotensin II and aldosterone. Primarily it is regulated by the rate of renal blood flow.
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11
Q

RAAS process

A
  1. Blood pressure falls which stimulates the juxta cells to secrete renin
  2. Renin converts angiotensinogen to Angiotensin I
  3. Angiotensin I is converted to angiotension II via angiotension converting enzyme
  4. Angiotension II acts on the adrenal cortex to stimulate aldosterone release and acts acts directly to raise blood pressure
  5. aldosterone released acts on kidneys to retain sodium, raising blood pressure
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12
Q

What does Ang II contribute to?

A

fluid and sodium balance

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13
Q

Ang II contribution at the brain

A
  • Stimulates vasopressin release at the hypothalamus
    • increases renal water reabsorption & restores blood volume/ pressure
  • Stimulates thirst and water intake
  • increases sympathetic outflow
    • increase CO, vasoconstriction, RAAS
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14
Q

Ang II contribution at vasculature

A
  • Vasoconstriction
    • short-term increase in blood pressure
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15
Q

Ang II contribution at the proximal tubule

A
  • stimulates apical Na-H-Exchanger (NHE)
    • stimulates salt & water reabsorption
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16
Q

ANP

A

Atrial Natriuretic Peptide

  • Increases sodium excretion
17
Q

Where does ANP come from?

A

Family of hormones released by cardiac cells

  • ANP from atria
  • Brain Natriureitc Peptide (BNP) from ventricles
18
Q

How does ANP increase Na excretion?

A
  • Induces natriuresis & diuresis - increase sodium and water excretion
    • also vasodilation
  • Released in high volume conditions in response to cardiac stretch
  • ANP dilates afferent arterioles & increases GFR
    • Also inhibits sodium reabsorption in the collecting duct
    • INhibits release of sodium/ water reabsorbing mediators