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Old 02-01-2012
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Question Site of action of Atrial Natriuretic Peptide

A patient with congestive heart failure presents with jugular venous distention, ascites, and peripheral edema. Blood work shows elevated levels of plasma atrial natriuretic peptide (ANP). ANP decreases Na+ reabsorption within which of the following?
A. The proximal tubule
B. The thick ascending limb of Henle's loop
C. The distal convoluted tubule
D. The cortical collecting duct
E. The inner medullary collecting duct
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  #2  
Old 02-01-2012
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Well, its collecting duct, where ANP will oppose Aldosterone action.

But what part of the collecting duct?! I guess medullary? E?

Where do u take these hardcore questions from?
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Old 02-01-2012
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ANP works in a way similar to amiloride, inhibits the ENaC, ( expressed on both the distal tubule and the collecting ducts)
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Old 02-01-2012
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Ans ........D .......

cortical CD for aldosterone and medullary for ADH ...
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Old 02-01-2012
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got it wrong.. wud hv picked PCT if the question wud hv been on my test!
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I think its A.... since its works within the proximal tubule inhibiting the Na-H exchanger
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I would choose A
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Old 02-01-2012
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ANP constricts the efferent arteriole and dialates the afferent arteriole.
Also it counteracts the effect of aldosterone to inhibit Na+ reabsorption.

Since aldosterone works on the cortical collecting duct, i assume ANP will too.

my answer is D.
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Old 01-18-2013
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Default aldosterone receptor

adldosterone recepr is located in late DCT and cortical collecting duct so which answer to pick?
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Old 01-18-2013
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ans. D)
Decreases the sodium absorption in cortical collecting duct
while one theory betweeen ANP and ADH is:
ANP secreted from atrium in response to cel stretch as a result of volume expansion---ANP provides the -ve feedback against the ADH in CNS and kidney. medulary colecting duct is primary site of action of ADH thereby ANP acts on medulary colecting duct to inhibits the action of ADH....
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Last edited by neha_subh; 01-18-2013 at 04:45 AM.
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Old 01-18-2013
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A. The proximal tubule

ANP is released from the atria in response to stretch and exerts its action by:
1) increasing the GFR by dilating the afferent arteriole and constricting the efferent arteriole, the net result of which causes an increase in hydrostatic pressure and hence the kidney favors filteration.

2) It works on the proximal convoluted tubules to decrease Na rebsorption (diuretic effect, makes sense because thats where the majority of Na is reabsorbed). It also works on the Distal tubules, where 10% of Na is reabsorbed normally, but I believe its main diuresis role is at the PCT

3) inhibits ADH release as well as suppresses RAAS.
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Last edited by SarahM; 01-18-2013 at 05:56 AM.
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Old 01-26-2013
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Quote:
Originally Posted by SarahM View Post
A. The proximal tubule

ANP is released from the atria in response to stretch and exerts its action by:
1) increasing the GFR by dilating the afferent arteriole and constricting the efferent arteriole, the net result of which causes an increase in hydrostatic pressure and hence the kidney favors filteration.

2) It works on the proximal convoluted tubules to decrease Na rebsorption (diuretic effect, makes sense because thats where the majority of Na is reabsorbed). It also works on the Distal tubules, where 10% of Na is reabsorbed normally, but I believe its main diuresis role is at the PCT

3) inhibits ADH release as well as suppresses RAAS.


direct action thro cGMP phoshorylation enac resulting in na loss ( dct and cortical collecting duct) reabsorption at pct is more or less fixed and subject to little change in functional nephron
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Old 01-26-2013
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Quote:
Originally Posted by crusader View Post
direct action thro cGMP phoshorylation enac resulting in na loss ( dct and cortical collecting duct) reabsorption at pct is more or less fixed and subject to little change in functional nephron
so you're saying that the site of action is going to be at the DCT?
According to a kaplan question I did a while back, the site of action is at the PCT... Not that i don't believe you, but for sake of clarification, do u have a reference for your answer? I'd really appreciate it
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Old 01-26-2013
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Quote:
Originally Posted by SarahM View Post
so you're saying that the site of action is going to be at the DCT?
According to a kaplan question I did a while back, the site of action is at the PCT... Not that i don't believe you, but for sake of clarification, do u have a reference for your answer? I'd really appreciate it
wikipedia ANF hope it helps
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Old 01-26-2013
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Thank you. I stand corrected
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Old 01-26-2013
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Though ANP inhibits action of angio 2 at PCT and DCT..I think here the best would be to choose DCT..Since it's the main site of compensatory Na absorption if there is dec Na abs before the fluid reaches DCT..

So is DCT final correct answer?
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  #17  
Old 02-17-2013
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Post ANP

sarah is right
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  #18  
Old 02-17-2013
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Warning!

According to wikipedia

"ANP decreases sodium reabsorption in the distal convoluted tubule (interaction with NCC)[10] and cortical collecting duct of the nephron via guanosine 3',5'-cyclic monophosphate (cGMP) dependent phosphorylation of ENaC"

so it states that two answers of the five are right !!

A. The proximal tubule
B. The thick ascending limb of Henle's loop

C. The distal convoluted tubule
D. The cortical collecting duct

E. The inner medullary collecting duct
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  #19  
Old 02-17-2013
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Default Brain natriuretic peptide & atrial natriuretic peptide

Ans. A. The Proximal Tubule

Here's a little more information about Brain natriuretic peptide/Atrial natriuretic peptide:

- Brain natriuretic peptide & atrial natriuretic peptide both cause vasodilatation (decreased preload) & diuresis; both activate guanylate cyclease inducing an increase in cGMP.

- Increased mechanical loads (pressure and/or volume overload) can increase the sarcomere content & volume of individual myocytes (hypertrophy) = prolonged hemodynamic overload = volume overload increases the release of both atrial natriuretic peptide & brain natriuretic peptide, facilitating natriuresis & diuresis.

- cause vasodilation (decreased preload) & diuresis.

- BNP/ANP is elevated in patients w/ heart failure

- it is released by the ventricles when they are stretched as they often are in CHF from systolic dysfunction.

- Kidney: ANP dilates afferent arterioles, increasing the glomerular filtration rate & the urinary excretion of sodium & water. Additioally, ANP limits sodium reabsorption (in the proximal tubule & the inner medullary collecting duct) & inhibits renin secretion.

- Adrenal gland: ANP restricts aldosterone secretion, leading to an increase in sodium & water excretion by the kidneys.

- Blood vessels: ANP relaxes vascular smooth muscle in arateiroles & venules, producing vasodilation. It also increase capillary permeability, leading to fluid extravasation into the iterstitum & a decrease in circulating blood volume.
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Cardiovascular-, Endocrine-, Physiology-, Renal-, Step-1-Questions

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