JG cells vs Macula Densa - who wins?

[sv3]

---

Members don't see this ad.

So in response to low BP, JG cells start the process which results in angotensin II activation which constricts blood vessels, including the afferent arteriole supplying the nephron. Now, when filtrate osmolarity is low, the macula densa cells function to dilate the afferent arteriole.

Since to me it seems possible and likely (major assumption) that low BP and low filtrate osmolarity can occur together, so which effect wins out?
The JG cells will be reducing filtration (through angio's constrictive props)and the macula densa work to increase it...........so i'm not sure what to think?

thanks
sv3

 

[Charles_Carmichael]

I think you might be a little bit confused about the renal response to low BP. If I'm misreading you, I apologize, and you can skip the next few paragraphs where I explain the RAAS.

The renin-angiotensin-aldosterone system (RAAS) is activated by both a decrease in renal perfusion pressure (which would be a result of low BP) and a decrease in concentration of NaCl at the distal tubule (which stimulates the macula densa and causes these cells to, in turn, stimulate the JG cells to secrete renin).

Both mechanisms (the JG cells sensing a drop in renal perfusion pressure via mechanoreceptors and the macula densa sensing a lower concentration of NaCl in the distal tubule) work together to stimulate renin secretion. A drop in concentration of NaCl at the distal tubule follows a drop in renal perfusion pressure (due to the drop in GFR).

Angiotensin II acts more strongly in constricting the efferent arteriole, not the afferent arteriole. Constricting the efferent arteriole would increase upstream pressure at the glomerulus, which would increase GFR. The macula densa acts to dilate the afferent arteriole via one mechanism; however, I'm not sure to what extent this dilation is. A second mechanism is that the macula densa stimulates renin secretion which results in ATII production, which, in turn, has a stronger vasoconstriction effect on the efferent arteriole; ATII also stimulates the release of aldosterone from the adrenal cortex.

Aldosterone cause Na+ reabsorption at the distal tubule, which increases plasma Na+ concentration. This increase in blood osmolarity triggers osmoreceptors in the hypothalamus which leads to ADH secretion from the posterior pituitary. ADH acts on the collecting duct to reabsorb water and increase blood volume. An increase in blood volume means that there's an increase in venous return, which then, due to the Frank-Starling mechanism, increases cardiac output. The increase in cardiac output combined with the increase in TPR due to ATII ultimately increases blood pressure. Remember, blood volume is the most important determinant of blood pressure.

That's the RAAS in a a nutshell, I guess.

So to answer your questions directly, yes low renal perfusion pressure and lower concentration of NaCl in the distal tubule occur together. However, I don't think they're competing against each other; rather, they work together to activate the RAAS and increase blood volume. The JG cells do NOT decrease GFR; the actions of ATII on the efferent arteriole are much greater than its actions on the afferent arteriole. The greater increase in resistance at the efferent arteriole would cause an increase in upstream pressure at the glomerulus; this means that GFR increases. The macula densa cells work the same way because they stimulate the JG cells to secrete renin; plus, they act via a second mechanism to dilate the afferent arteriole. Also, keep in mind that other mechanisms, such as an increase in thirst (due to ATII action on the hypothalamus), that try to compensate for the low BP and try to increase blood volume.

So the chain reaction set off by a low BP is pretty complex that involves many different types of cells, molecules, systems, etc. working together to compensate and try to increase BP rather than each thing working independently (ie. drop in BP causes both the secretion of renin and dilation of the afferent arteriole due to the macula densa; then, the result of renin, ATII, increases TPR and causes greater increase in resistance at the efferent arteriole while also increasing thirst). Rather than trying to think of each mechanism as acting on its own, I think it's helpful to understand the mechanism's role in the overall response to a certain condition, such as low BP. Do you see what I'm saying?

Hope this helps.

 

[sv3]

I think you might be a little bit confused about the renal response to low BP. If I'm misreading you, I apologize, and you can skip the next few paragraphs where I explain the RAAS.

The renin-angiotensin-aldosterone system (RAAS) is activated by both a decrease in renal perfusion pressure (which would be a result of low BP) and a decrease in concentration of NaCl at the distal tubule (which stimulates the macula densa and causes these cells to, in turn, stimulate the JG cells to secrete renin).

Both mechanisms (the JG cells sensing a drop in renal perfusion pressure via mechanoreceptors and the macula densa sensing a lower concentration of NaCl in the distal tubule) work together to stimulate renin secretion. A drop in concentration of NaCl at the distal tubule follows a drop in renal perfusion pressure (due to the drop in GFR).

Angiotensin II acts more strongly in constricting the efferent arteriole, not the afferent arteriole. Constricting the efferent arteriole would increase upstream pressure at the glomerulus, which would increase GFR. The macula densa acts to dilate the afferent arteriole via one mechanism; however, I'm not sure to what extent this dilation is. A second mechanism is that the macula densa stimulates renin secretion which results in ATII production, which, in turn, has a stronger vasoconstriction effect on the efferent arteriole; ATII also stimulates the release of aldosterone from the adrenal cortex.

Aldosterone cause Na+ reabsorption at the distal tubule, which increases plasma Na+ concentration. This increase in blood osmolarity triggers osmoreceptors in the hypothalamus which leads to ADH secretion from the posterior pituitary. ADH acts on the collecting duct to reabsorb water and increase blood volume. An increase in blood volume means that there's an increase in venous return, which then, due to the Frank-Starling mechanism, increases cardiac output. The increase in cardiac output combined with the increase in TPR due to ATII ultimately increases blood pressure. Remember, blood volume is the most important determinant of blood pressure.

That's the RAAS in a a nutshell, I guess.

So to answer your questions directly, yes low renal perfusion pressure and lower concentration of NaCl in the distal tubule occur together. However, I don't think they're competing against each other; rather, they work together to activate the RAAS. The JG cells do NOT decrease GFR; the actions of ATII on the efferent arteriole are much greater than its actions on the afferent arteriole. The greater increase in resistance at the efferent arteriole would cause an increase in upstream pressure at the glomerulus; this means that GFR increases. The macula densa cells work the same way because they stimulate the JG cells to secrete renin; plus, they act via a second mechanism to dilate the afferent arteriole. Also, keep in mind that other mechanisms, such as an increase in thirst (due to ATII action on the hypothalamus), that try to compensate for the low BP and try to increase blood volume.

Hope this helps.

thanks very much, it helps in that it all makes sense but totally contradicts what i've read in TPR....hence my confusion. You answer makes more sense though at least to me and i can put things together now. TPR stated (I've tripled checked) Angio II constricts the afferent, this way, less blood is filtered and thus helps maintain more blood in the circulation when blood volume is low (the question was about significant blood loss). Sounds sketch to me but its what they say. So in effect, if blood volume is low, TPR states you want to decrease the filtration rate and that Angio II does this by constricting the afferent arteriole. I can see their point but this could cause so many more issues and doesn't seem like the best reaction. So that's why i thought the JG and Macula densa opposed........and that just didn't make sense. I'll go with what you said........TPR doesn't make many errors but in this case i cant make sense of it.

thanks very much

EDIT: reread your reply, very nice, sunk in well, and cleared this up nicely. it was my last passage before i do the AAMCs so kinda threw me off.

 

[Charles_Carmichael]

It's a weird explanation that TPR gave, but ATII does constrict the afferent arteriole also. However, it's actions on the efferent are much, much greater. So, while the constriction of the afferent arteriole slightly decreases GFR (since the actions of ATII on the afferent arteriole are minimal), the greater increase in resistance at the efferent arteriole increases the pressure upstream (at the glomerulus), which more than makes up for the slight decrease in GFR due to afferent constriction. The overall result is that GFR either remains the same or increases; it definitely does not decrease.

As a point of interest, sympathetic activity has a much greater effect on the afferent arteriole compared to the efferent (which has fewer adrenergic receptors). So, if sympathetic stimulation is involved, GFR decreases due to the greater increase in resistance at the afferent arteriole compared to the efferent (which cannot compensate for the decrease in pressure at the glomerulus).

So, if in your passage, sympathetic stimulation was also involved (if the hemorrhage was significant), I can see a decrease in GFR occurring. However, I don't know at what point sympathetic activity outweighs the actions of ATII in order to decrease GFR. Hope this helps.

 

[Grosenbe]

A little input...

The effect of increasing vasoconstriction that you read may be totally unrelated to filtration. Vasocontriction increases total peripheral resistance. This is important because it leads to an increase in mean arteriole pressure. This is an essential part of cardiac compensation for decreased blood volume.