Renin angiotensin system I don't understand?

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In summary: The body wants to preserve water and electrolytes.So in summary, the MD understands that if there is a loss of fluid, plasma NaCl will be normal. However, since both NaCl and water filtration are decreased, nacl reaching the macula densa will be normal. The MD also understands that if there is a high GFR, there is lots of proteins in peritubular capillary fluid and they can increase reabsorption of sodium. However, since 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?From your original question, the MD understands that if
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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 :smile:

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?
 
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Look into flow rates and how that might affect what the macula densa "sees".
 
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bobze said:
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.
 
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sameeralord said:
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)

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".
 
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Hello,

The renin angiotensin system is a complex process that helps to regulate blood pressure and fluid balance in the body. It involves the release of renin, an enzyme produced by the kidneys, in response to changes in sodium chloride (NaCl) levels. The macula densa is a group of specialized cells in the kidney that monitor the NaCl concentration in the fluid flowing through the distal tubule.

In response to a loss of fluid from the body, the NaCl concentration in the fluid reaching the macula densa would be normal. This would not significantly affect the macula densa, as its main role is to detect changes in NaCl concentration and trigger the release of renin if needed.

As for your question about glomerulotubular balance, this is a mechanism that helps to maintain a balance between the amount of sodium and water reabsorbed by the kidneys. When there is a high GFR (glomerular filtration rate), there is a higher rate of fluid and solute flow through the tubules. This results in increased reabsorption of sodium and water in the proximal tubule, leading to a decrease in the amount of sodium and water reaching the distal tubule. This helps to maintain a balance and prevent excessive loss of sodium and water from the body.

On the other hand, when there is a decreased GFR, there is a lower rate of fluid and solute flow through the tubules. This results in a decrease in reabsorption of sodium and water in the proximal tubule, allowing more sodium and water to reach the distal tubule. This helps to maintain a balance and prevent excessive retention of sodium and water in the body.

I hope this helps to clarify your understanding of the renin angiotensin system and glomerulotubular balance. Let me know if you have any other questions. Keep up the curiosity and keep learning!
 

What is the Renin-Angiotensin System?

The Renin-Angiotensin System (RAS) is a hormone system in the body that helps regulate blood pressure and fluid balance. It is primarily composed of the hormone renin, which is produced by the kidneys, and the peptide angiotensin, which is converted from angiotensinogen by the enzyme renin.

How does the Renin-Angiotensin System work?

The RAS works by responding to changes in blood pressure and fluid balance. When blood pressure drops, the kidneys release renin into the bloodstream. Renin then converts angiotensinogen into angiotensin I. An enzyme called angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, which causes blood vessels to constrict and increases blood pressure. Angiotensin II also stimulates the release of aldosterone, a hormone that helps regulate fluid and electrolyte balance in the body.

What is the role of the Renin-Angiotensin System in hypertension?

In hypertension (high blood pressure), the RAS is overactive, causing blood vessels to constrict and increasing blood pressure. This can lead to serious health issues such as heart disease, stroke, and kidney disease. Medications that target the RAS, such as ACE inhibitors and angiotensin receptor blockers (ARBs), are often prescribed to help lower blood pressure and reduce the risk of these health issues.

How is the Renin-Angiotensin System regulated?

The RAS is regulated by a negative feedback loop. When blood pressure and fluid balance are restored, the body signals the RAS to decrease its activity. This is achieved by inhibiting the release of renin and decreasing the production of angiotensin II. This feedback loop helps maintain homeostasis and prevent excessive constriction of blood vessels.

What are the clinical implications of dysregulation in the Renin-Angiotensin System?

Dysregulation in the RAS can lead to various health issues, including hypertension, heart disease, stroke, and kidney disease. It has also been linked to other conditions such as diabetes, metabolic syndrome, and obesity. Understanding and targeting the RAS is crucial in managing and treating these conditions and improving overall health outcomes.

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