Renin angiotensin system I don't understand?

[sameeralord]

Hello everyone,

So in renin angiotensin system, the NaCl concentration reaching the macula densa is monitored. Now my question if if there is loss of fluid from the body and both NaCl and water is lost from the body,plasma NaCl would be normal, now how would this affect macula densa. Okay so GFR decreases, but both NaCl and water filtration is decreased, so nacl reaching macula densa would be normal. I know I have really confused myself and I nedd some help. Thanks

EDIT: Ok now I understand it is to do with glomerulotubular balance. But now I don't undertand that. Ok if there is high GFR, there is lots of proteins in peritubular capillary fluid and they can increase reabsorption of sodium. But sodium moves out tubular cells via active transport so how can this work? If there is decreased GFR how does glomerulotubular balance decrease sodium reabsorption?

 

[bobze]

Look into flow rates and how that might affect what the macula densa "sees".

 

[sameeralord]

Look into flow rates and how that might affect what the macula densa "sees".

Hello Bobze. Ok if there is high GFR, flow rate would be high and there would be less absorption and vise versa. But what I'm saying is sodium moves into tubular cell passvely, then moves out of the cell actively and requires ATP. So how can these things have any effect, if sodium is reabsorbed actively. Also if there is high GFR and there is less absorption, then tubuloglomerulr balance would not be maintained.

 

[bobze]

Hello Bobze. Ok if there is high GFR, flow rate would be high and there would be less absorption and vise versa. But what I'm saying is sodium moves into tubular cell passvely, then moves out of the cell actively and requires ATP. So how can these things have any effect, if sodium is reabsorbed actively. Also if there is high GFR and there is less absorption, then tubuloglomerulr balance would not be maintained.

From your original question;

Now my question if if there is loss of fluid from the body and both NaCl and water is lost from the body,plasma NaCl would be normal, now how would this affect macula densa. Okay so GFR decreases, but both NaCl and water filtration is decreased, so nacl reaching macula densa would be normal. I know I have really confused myself and I nedd some help.

So if you have an isoosmotic volume loss, what happens to the amount of fluid entering the tubule? Does it increase or decrease?

If it decreases, then what does (regarding electrolytes, particularly that all important one Na+) macula densa "see" per unit time? Does it "see" more sodium? Less? The same amount?

What is the MD's response to more sodium? What is the response to less?

Then apply what you know of the RAA (renin-angiotensin-aldosterone) system and how that affects the; afferent and/or efferent vessels, the BP, the blood volume etc.

When you solve clinical problems or think about clinical problems Sameer, use a system to get you to the answer.

Remember that our bodies are millions of years in the making and are very good problem solvers. Not much, isn't there for a reason or doesn't help to maintain a "normal" state for us.

So when you look at a problem like "isoosmotic loss of fluid" ask yourself "what does the body want to do", "how will it correct this problem". Answer that, then "reverse-engineer" yourself to through the problem.

Spoiler (try and solve it yourself, you'll learn it better that way, but if you get stuck look at the spoiler below)

Spoiler

So when the body looses an isoosmotic amount of fluid it says "I need to raise the fluid levels back up to full". How does it do this?

We can't actively absorb water, we get more water by keeping more salt. So the MD releases renin. The renin acts on angiotensinogen to make AI. ACE in the kidney and the lung make AI into AII (or plain ol' angiotensin).

AII then does four big things for the body to bring the fluid level back up;

1. It stimulates production of aldosterone from the zona glomerulosa of the adrenal cortex. Aldo acts on NCC channels in the DCT and ENaC channels in principle CD cells, to increase Na reabsorption; water follows

2. It acts directly on NHE3 channels in the PCT (S1 regions) to increase Na reabsorption; water follows.

3. It stimulates the posterior pituitary to release ADH (vassopressin) which increases thirst, which gets us more water to follow the increased Na reabsorption. It also increases AQP2 channels throughout the distal tubule; now even more water can follow.

4. It causes vasoconstriction in the efferent arterioles, which raises the GFR back up to normal levels and increases kidney function. Think about it like a bridge, where on the "efferent end" (leaving end) it goes down from 4 lanes to 2. This causes a "traffic jam" back on the bridge--raising the "bridge's filtration pressure".