Regulate Sodium Balance
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Questions and Answers

Which of the following accurately describes the kidney's regulatory response to decreased sodium levels?

  • Decreased activity of the Na/K ATPase on the basolateral membrane of proximal tubule cells.
  • Increased vasoconstriction of the efferent arteriole.
  • Reduced activity of the Na/H exchanger on the luminal membrane.
  • Reduced release of atrial natriuretic peptide (ANP). (correct)

How does Angiotensin II affect glomerular filtration rate (GFR) when it induces vasoconstriction in both the afferent and efferent arterioles?

  • GFR decreases because the reduced blood flow into the nephrons outweighs any increase in filtration pressure. (correct)
  • GFR initially increases but then decreases due to prolonged vasoconstriction.
  • GFR remains unchanged as vasoconstriction effects cancel each other out.
  • GFR increases due to enhanced pressure in the glomerulus.

In response to increased sodium levels, how does the body adjust fluid volume and sodium excretion through hormonal regulation?

  • Stimulates aldosterone secretion, which reduces sodium excretion and maintains ECF volume.
  • Inhibits the RAAS pathway and increases atrial natriuretic peptide (ANP) release, promoting sodium excretion and decreasing ECF volume. (correct)
  • Activates the RAAS pathway, leading to increased sodium retention and decreased ECF volume.
  • Enhances angiotensin II production, causing vasoconstriction and increased sodium reabsorption.

Which of the following correctly links a specific physiological response to the activation of the RAAS pathway?

<p>Increased Na/H exchanger activity on the luminal membrane enhances Na+ reabsorption. (D)</p> Signup and view all the answers

What is the combined effect of Angiotensin II induced vasoconstriction of both afferent and efferent arterioles on sodium excretion?

<p>Decreases sodium excretion by reducing GFR despite increased filtration pressure. (C)</p> Signup and view all the answers

How does increased activity of the Na/K ATPase on the basolateral membrane of proximal tubule cells contribute to sodium balance?

<p>It increases sodium reabsorption into the interstitial fluid, leading to decreased sodium excretion. (B)</p> Signup and view all the answers

Which of the following is an accurate description of how the body responds when sodium levels are excessively high?

<p>Increased release of ANP inhibits sodium reabsorption, helping to lower sodium levels. (B)</p> Signup and view all the answers

How does angiotensin II affect the ECF volume through its direct effects on renal function?

<p>Increases ECF volume by decreasing sodium excretion. (D)</p> Signup and view all the answers

Predict the outcome if a patient with chronically elevated sodium levels also has a condition that impairs ANP release.

<p>Further increase in sodium levels and ECF volume due to reduced sodium excretion. (C)</p> Signup and view all the answers

In a scenario of low blood pressure, how would the body adjust sodium handling to restore blood pressure?

<p>Increase activity of the RAAS pathway to enhance sodium and water reabsorption. (C)</p> Signup and view all the answers

How does Atrial Natriuretic Peptide (ANP) counteract the effects of aldosterone on sodium reabsorption in the kidneys?

<p>By directly inhibiting sodium channels in the distal convoluted tubule and collecting duct, reducing sodium reuptake. (D)</p> Signup and view all the answers

What is the primary mechanism by which angiotensin-converting enzyme (ACE) contributes to blood pressure regulation?

<p>It catalyzes the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and stimulator of aldosterone release. (B)</p> Signup and view all the answers

How do baroreceptors in the aortic arch contribute to the regulation of renin release from juxtaglomerular cells?

<p>By detecting changes in blood pressure and signaling the cardiovascular center in the medulla oblongata, which in turn modulates juxtaglomerular cell activity. (D)</p> Signup and view all the answers

How does increased GFR, resulting from ANP-induced vasodilation of the afferent arteriole, lead to increased sodium excretion?

<p>The faster filtrate flow reduces the opportunity for sodium reabsorption in the tubules, resulting in more sodium being excreted. (C)</p> Signup and view all the answers

What is the relationship between the actions of ANP and aldosterone regarding sodium balance and blood pressure?

<p>ANP and aldosterone have opposing effects; ANP promotes sodium excretion and lowers blood pressure, while aldosterone promotes sodium retention and raises blood pressure. (B)</p> Signup and view all the answers

How do the macula densa cells respond to decreased sodium levels in the filtrate, and how does this response contribute to maintaining sodium balance?

<p>They secrete a paracrine factor that stimulates renin secretion from the juxtaglomerular cells, ultimately increasing sodium reabsorption. (B)</p> Signup and view all the answers

In what way does the cardiovascular center in the medulla oblongata integrate signals from baroreceptors and influence kidney function to maintain blood pressure?

<p>By modulating sympathetic nerve activity to the kidneys, thereby influencing renin release and sodium reabsorption. (A)</p> Signup and view all the answers

What would be the expected physiological response to a sudden increase in blood volume regarding ANP and the renin-angiotensin-aldosterone system?

<p>Increased ANP release, decreased renin secretion, leading to increased sodium excretion. (C)</p> Signup and view all the answers

What are the consequences of blocking the action of ACE (angiotensin-converting enzyme) in a patient with hypertension?

<p>Decreased levels of angiotensin II, promotion of vasodilation, and reduced aldosterone release. (A)</p> Signup and view all the answers

How does the length of angiotensinogen, angiotensin I, and angiotensin II peptides relate to their function in the renin-angiotensin-aldosterone system?

<p>The specific length and structure of each peptide are critical; Angiotensin II's shorter length is essential for binding to its receptors and exerting its potent effects. (C)</p> Signup and view all the answers

Flashcards

Kidney's Role in Na+ Balance

The kidney regulates sodium (Na+) balance by adjusting excretion to maintain homeostasis.

Low Na+ Triggers...

Low sodium levels activate the renin-angiotensin-aldosterone system (RAAS).

High Na+ Triggers...

High sodium levels suppress the RAAS pathway and stimulate the release of atrial natriuretic peptide (ANP).

Na+ Effect on Blood Volume

Increased sodium leads to increased ECF volume, raising total blood volume.

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RAAS Products

The RAAS pathway produces renin and two hormones: angiotensin II and aldosterone.

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Angiotensin II's Action

Angiotensin II increases Na+/H+ exchanger activity, enhancing Na+ reabsorption in tubule cells.

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Na+/K+ ATPase Role

Increased Na+/K+ ATPase activity by Angiotensin II moves more Na+ from tubule cells into interstitial fluid, for reabsorption by blood vessels.

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Afferent Arteriole Constriction

Angiotensin II causes vasoconstriction of the afferent arteriole, decreasing GFR and reducing Na+ excretion.

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Both Arterioles Constricted

Angiotensin II constricts both afferent and efferent arterioles, resulting in a net reduction of GFR.

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Angiotensin II as Vasoconstrictor

Angiotensin II is a potent vasoconstrictor, leading to decreased GFR and reduced fluid (including sodium) excretion.

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Renin

An enzyme secreted by juxtaglomerular cells in response to low sodium levels or low blood pressure. It initiates the renin-angiotensin-aldosterone system (RAAS).

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Angiotensinogen

A protein produced by the liver that is cleaved by renin to form angiotensin I.

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Angiotensin I

A peptide formed from angiotensinogen by renin, converted to angiotensin II by ACE.

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Angiotensin-Converting Enzyme (ACE)

An enzyme that converts angiotensin I to angiotensin II, primarily in the lungs.

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Angiotensin II

A potent hormone that causes vasoconstriction, stimulates aldosterone release, and increases sodium reabsorption.

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Macula Densa Cells

Detect changes in filtrate composition to regulate renin secretion.

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Baroreceptors

Located in the aortic arch and connect to the cardiovascular center in the medulla oblongata to detect blood pressure.

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Atrial Natriuretic Peptide (ANP)

A protein made by cardiac atrial cells, released when blood volume and pressure increase.

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Actions of ANP

ANP prevents aldosterone actions and increases GFR.

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ANP's effect on GFR

ANP vasolidates the afferent arteriole, increasing GFR

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Study Notes

  • The kidney maintains sodium balance and can alter excretion to maintain homeostasis

Sodium Levels

  • Low sodium levels activate the renin-angiotensin-aldosterone system (RAAS), releasing angiotensin II and aldosterone
  • High sodium levels decrease the RAAS pathway and release atrial natriuretic peptide (ANP)
  • Increased sodium concentration increases extracellular fluid (ECF) volume, and increases total blood volume

RAAS Pathway

  • Produces the enzyme renin and the hormones angiotensin II and aldosterone
  • Juxtaglomerular cells produce Renin in response to low sodium levels
  • Liver creates the protein angiotensinogen
  • Renin splits angiotensinogen (452 amino acids long) into angiotensin I (10 amino acids long)
  • Angiotensin I is cleaved again by angiotensin-converting enzyme (ACE) into angiotensin II (8 amino acids long)

Control of Renin Release

  • Chemoreceptors on the macula densa cells detect the filtrate composition
  • Baroreceptors located on the aortic arch connect to the cardiovascular center in the medulla oblongata and innervate the juxtaglomerular cells in the kidney
  • Low sodium levels cause macula densa cells to secrete a chemical messenger (paracrine factor), causing the nearby juxtaglomerular cells to secrete renin

Angiotensin

  • Increases Na/H exchanger activity on the luminal membrane, increasing Na and H movement from filtrate into tubule cells
  • Increases Na/K ATPase activity on the basolateral membrane, resulting in increased Na excretion from proximal tubule cells into interstitial fluid, which is reabsorbed by nearby blood vessels
  • Angiotensin II is a vasoconstrictor, vasoconstriction of the afferent arteriole results in decreased glomerular filtration rate (GFR), reducing filtration production, and reducing sodium excretion
  • Vasoconstriction of the efferent arteriole at the same time results in decreased GFR because so little blood ends up entering the corpuscles of nephrons when the afferent arteriole is already vasoconstricted

ANP

  • Cardiac atrial cells produce and release ANP into the blood
  • Increased blood volume and pressure stretches the atrial cells
  • Atrial cells contain mechanoreceptors that detect stretching, which releases ANP into the blood

ANP Actions

  • Prevents the actions of aldosterone and blocks aldosterone release from the adrenal gland
  • Increases GFR: ANP causes the afferent arteriole to vasodilate, increasing GFR, so more filtrate is produced and travels faster
  • Less opportunity for Na to be reabsorbed, so more is excreted

Control of Aldosterone Release

  • Aldosterone is a steroid released by the adrenal gland (endocrine tissue on top of the kidney)
  • Angiotensin II and/or high levels of potassium are stimuli for aldosterone

Aldosterone

  • Sodium channels increase on the luminal membrane of principle cells, allowing for more movement of Na from filtrate into tubule cells
  • Na/K ATPase activity increases transporting Na out into interstitium and into blood vessels
  • Potassium channels can increase on the luminal membrane

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Sodium Balance Regulation PDF

Description

The kidney is responsible for maintaining sodium balance in the body by altering excretion to maintain homeostasis. Low sodium activates the renin-angiotensin-aldosterone system (RAAS), releasing angiotensin II and aldosterone. High sodium decreases the RAAS pathway and releases atrial natriuretic peptide (ANP).

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