Can anybody help me out with the JGA (inconsistency between FA and Costanzo).

[TheShaker]

FA is telling me that the macula densa senses NaCl at the DCT and reacts accordingly by adjusting the release of renin, affecting RAAS, and affecting ATII action at the efferent arteriole.

Costanzo says something different in that the macula densa senses NaCl at the DCT and then releases some kind of effector to the afferent arteriole to cause vasoconstriction, completely different from what FA says.

I'm not quite sure which one to believe, but FA is somewhat sketchy in that it has a lot of errors (this was not found in the errata list).

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[zhopv10]

The macula densa is specialized epithelium that touches the afferent and I believe efferent arteriole a of the glomerulus that it arose from and makes the start of the DCT and is part of it. It utilizes purinergic signaling in response to elevated sodium and leads to a series of signals (local) that constrict the afferent arteriole. Decreased sodium levels leads to release of sodium and prostaglandins that dilate the afferent arteriole. Now the juxtaglomerular cells are in the afferent arteriole and they release renin in response to b1 stimulation, decreased perfusion, and decreased NaCl. These two types of cells and the mesangial cells make up the JGA. Perhaps this is where the confusion/source conflict arises from? Because both functions are indeed going on in the general region but by different cell types in different parts of the structure.


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[TheShaker]

The macula densa is specialized epithelium that touches the afferent and I believe efferent arteriole a of the glomerulus that it arose from and makes the start of the DCT and is part of it. It utilizes purinergic signaling in response to elevated sodium and leads to a series of signals (local) that constrict the afferent arteriole. Decreased sodium levels leads to release of sodium and prostaglandins that dilate the afferent arteriole. Now the juxtaglomerular cells are in the afferent arteriole and they release renin in response to b1 stimulation, decreased perfusion, and decreased NaCl. These two types of cells and the mesangial cells make up the JGA. Perhaps this is where the confusion/source conflict arises from? Because both functions are indeed going on in the general region but by different cell types in different parts of the structure.


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I understand that the JG cells and macula densa are two different populations of cells. FA actually directly states that it's the macula densa doing this.

"Macula densa cells sense decreased NaCl delivery to DCT --> increased renin release --> efferent arteriole vasoconstriciton --> increased GFR." (direct quote from FA 2016, pg. 540)

 

[zhopv10]

Dang ya FA is def wrong then, cause ya it's the juxtaglomerular cells releasing the renin and the macula densa doing the local control via purine signaling and such


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[teehees]

I'm more concerned about the afferent vs efferent irregularity. Which is a huge difference,

So far i've solved questions successfully under the efferent assumption so i'll stick with that

 

[worldbeater]

Anytime you are deciding between FA and an actual professor of physiology like Costanzo, go with the prof. She's correct according to World and what I was taught. The macula densa is located right after thick ascending loop of henle, it's job is to sense volume depletion. If this occurs, it sends a signal (I don't know how), to the juxtaglomerular apparatus, who's purpose is to start the whole RAAS pathway. The JG apparatus is located on the afferent artery (World Q), wraps around the DCT, and hypertrophies through smooth muscle (World Q), sending renin on it's journey to start a cascading pathway to ultimately push aldosterone and drag 1 ion of Na+/3 ions of water into the serum to increase the blood pressure.

Also, to note in a low-volume state, RAAS happens only after 20 minutes. 0-2 seconds is your carotid reflex, 2 seconds-20 minutes is constriction of your alpha 1 receptors in your veins.

 

[teehees]

I was referring to the fact he said ?angiotensin ii constricts the afferent instead of efferent as mentioned in first aid

 

[worldbeater]

I was referring to the fact he said ?angiotensin ii constricts the afferent instead of efferent as mentioned in first aid

Angiotensin II constricts both the afferent and efferent, but has a greater effect on the efferent. This causes a backpedaling of volume down to the GFR and increases it.

It's a tricky concept, different sources don't write the full line like I did above and are therefore incomplete, which makes it confusing for the student understand it.

 

[zhopv10]

I was referring to the fact he said ?angiotensin ii constricts the afferent instead of efferent as mentioned in first aid

Not sure if this was directed at me but I said the adenosine/purine/prostaglandin signaling went to the afferent arteriole (dilation), angiotensin II works as worldbeater said: on both preferentially on the efferent. Sorry if I didn't make that clear.


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[Kazaki]

The way I understand it is that there's dual function. The macula dense senses the rise or fall of NaCl..
Rise in NaCl (in other words, a rise in RBF) causes the release of adenosine to constrict the afferent. Fall in NaCl activates the RAAS, which constricts the efferent.

 

[Transposony]

 

[Transposony]

Macula densa cells sense ↑NaCl delivery to DCT Ž→ adenosine release Ž→ afferent arteriolar constrictionŽ → ↓GFR

Macula densa cells sense ↓NaCl delivery to DCT Ž→ renin release (JG Cells) → efferent arteriolar constriction (via AT II) Ž→ ↑GFR

 

[Entadus]

Macula densa cells sense ↑NaCl delivery to DCT Ž→ adenosine release Ž→ afferent arteriolar constrictionŽ → ↓GFR

Macula densa cells sense ↓NaCl delivery to DCT Ž→ renin release (JG Cells) → efferent arteriolar constriction (via AT II) Ž→ ↑GFR

Excellent!

The first case we'd call "Tubuloglomerular feedback"
The second case is the primary physiologic response of the Juxtaglomerular apparatus (initiates the R.A.A. axis)

 

[worldbeater]

Macula densa cells sense ↑NaCl delivery to DCT Ž→ adenosine release Ž→ afferent arteriolar constrictionŽ → ↓GFR

So I didn't know this. Have you guys seen a practice question on this before?

 

[Entadus]

So I didn't know this. Have you guys seen a practice question on this before?

p. 253 of Costanzo is the only place I've seen it... but I have barely scratched the surface of UWorld

 

[Kazaki]

p. 253 of Costanzo is the only place I've seen it... but I have barely scratched the surface of UWorld

I recently got a question on Kaptest that asked about this in an indirect way. Something to do with acetozolamide and how it causes more NaCl to reach the macula dense therefore it constricts the afferent. Nice question