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  1. #1
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    Need Help with kidney phsyio.

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    Does anyone know why ADH is less effcetive in reabsorbing water at the collecting duct if less than two-thirds of Fluid is reabsorbed in the prox. tubule? (Example given was an uncontrolled diabetic)

    I think I am having problem with how the gradient btw medulla and the tubular lumen is established in the first place. I understand that osm of fluid in tubule is 300 in PCT. As we move into the ascending limb it becomes 600 mosm because of diffusion of water and Na plus other elctrolytes being left behind. and at the tip of henle it becomes 1200 mosm. and so on (are these number the normal physiology of osm in the medullary interstitium? and Does the tubular osmol try to become the same as the medullary interstitial osmolarity as fluid mover thru the segments?)
    I also undertand that if less than 2/3 of fluid is reabsorbed at PCT (less absorption of glucoe or Na means that the water also hangs on to it and as you go down to the ascending limb there will be less diffusion of water and I guess the osm in the tubule will be less versus the interstitium ? What does it exactly mean the transporter become overwhelmed (mechanism?) How does that effect the medullary interstitium and ADH at the collecting duct?
    Can someone explain this concept to me plaese.

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    transport maximum

    1. You asked: What does it exactly mean the transporter becomes overwhelmed (mechanism?)
    I think it is biochemistry. You know from biochemistry that many enzymes (and other proteins, like transporters) obey Michaelis-Mantene's kinetics. They have Km and Vmax. In physiology, Km has the sense of affinity for some substance, and Vmax is transport maximum (capacity). For more details, see in any biochemistry book (enzymology).
    2. You also asked: Does anyone know why ADH is less effective in reabsorbing water at the collecting duct if less than two-thirds of Fluid is reabsorbed in the prox. tubule? (Example given was an uncontrolled diabetic)
    I think that in case of uncontrolled diabettes mellitus, we have so called osmotis diuresis. (Recall that there are two things: water diuresis and osmotic diuresis). Glucose is osmotic active substance, so it drags water. Also, if there is too much glucose in tubular fluid, then, osmolarity of tubular fluid is increased so the osmotic gradient between tubular fluid and medullar interstitium is decreased so less water can be reapsorbed.Recall that there are two conditions to be fulfiled in order to be able to concentrate the urin:1. presence of ADH (which will insert water canals)2. hyperosmolarity of medullar interstitium (You can't do anything with ADH only, because there is no active water transport, but water is transported by osmosis, and main thing necessary for osmosis is osmotic gradient - difference in osmolarity between tubuar fluid and medullar interstitium).How is made hyperosmolarity of medullar interstitium? By countercurrent system which consists of countercurrent multiplier (loop of Henle) and countercurrent exchanger (vasa recta).I hope I succeeded to help you at least a little.

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    Could you tell me in detail how the osmolarity changes starting at PCT down to Collecting duct if less than 2/3 of electrolytea and water are being reabsorbed in the PCT. How does the Osmolarity change in tubule and interstitium as well as Vasa recta as you go from PCT to descending to ascending ti distal and collecting duct and how the final interstitial osmolarity affect the action of ADH. I would very much appreciate it. If I know those details I can undertand this problem.

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    Let's try. I must say that I can't explain it so good, because maybe it is not so clear to me either. In glomerulus, we have blood (osmolarity about 300 mOsm/l). Then, we have filtration, and filtered fluid which comes to PCT has the same osmolarity as plasma (why? because ions and water are filtrated in the same ratio). Then, in PCT we have isoosmotic reapsorption which means that, again, water and solutes are reapsorbed in the same ratio. So, in PCT osmolarity remains 300 mOsm/l.Then, we come to descending limb of loop of Henle in which only water is reapsorbed but not the solutes (it is because the membranes of those cells lining descending limb of loop of Henle aren't permeable to solutes, and are very permeable to water), so as the water is being reapsorbed, the osmolarity is becoming higher and higher. You know that water is reapsorbed by osmosis. The main thing necessary for osmosis is osmotic gradient, that is to say difference between osmolarity of tubular fluid and medullar interstitium (why I said medullar? because the loop of Henle is located in renal medulla, of course it refers to so called juxtamedullar nephrons). So, reapsorption here depends only on osmotic gradient, so we can say on medullar interstitium osmolarity. Result: tubular fluid osmolarity rises up to 1200 mOsm/l if medullar interstitium osmolarity is 1200, or up to 1000 mOsm/l if medullar interstitium osmolarity is 1000 (osmosis is equilibrating osmolarity of tubular fluid and medulla).Then, we come to ascending limb of the loop of Henle which has thin and thick segment (thin segment has only passive transport, and thick segment has active transport). Here, contrary to the descending limb, only solutes (ions: Na, Cl, Mg, Ca...) are reapsorbed but not the water. So, you can guess what happens to tubular fluid osmolarity. Osmolarity decreases (two reasons: first because ions are reapsorbed, second because water isn't reapsorbed), and when come to the end of the loop of Henle tubular fluid osmolarity is about 100 mOsm/l (that is why this part of nephron is called dilution segment).All things that I tried to explain by now, they are called OBLIGATED REAPSORPTION. This means it is always like that. And, now, we think, how can we get the urine with osmolarity from 100 to 1200 mOsm/l?! This is thanks to DCT and collecting duct where FACULTATIVE REAPSORPTION is done. This means it is done only if necessary (only in presence of some hormones that are secreted on specific stimuli).So, if there is much ADH, we will reapsorb more water, and urine will become more concentrated. If there is no ADH, we can't reapsorb water, so the urine osmolarity will stay 100 mOsm/l like it was on the top of loop of Henle. Here, also there is facultative reapsorption of sodium (aldosterone), calcium (PTH, calcitonin, D3),...And, now, which is the highest possible urine osmolarity? It depends on two factors:1. presence of ADH2. osmotic gradient (because water is reapsorbed by osmosis)Presence of ADH is only when there are stimuli for its secretion (hypovolemia, decreased blood pressure, plasma hyperosmolarity). ADH will insert transporters for water in membranes, but it is not enough. Water goes by osmosis, so very important factor is medullar osmolarity. Medulla must have higher osmolarity than tubular fluid in order to reapsorb water (in order to allow osmosis which will then equilibrate osmolarity in collecting duct and in medulla). If we had much ADH but medullar interstitium had the same osmolarity like tubular fluid, there could not be any osmosis and we could throw ADH away and our urine couldn't be concentrated! But, if medulla has hyperosmolarity, then osmosis is possible!

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    vasa recta

    In previous messages, I have written everything I know about osmolarity and nephron.Now, about vasa recta.At the beginning of vasa recta, osmolarity of plasma is 300 mOsm.During the descending part, osmolarity increases because the medullar interstitium is also more and more concentrated, so vasa recta loses water (osmosis) and absorbs ions (passive diffusion of NaCl down its concentration gradient). If medullar interstitium has 1200 mOsm/l, then at the end of descending part of vasa recta, osmolarity would be also 1200.During the ascending part of vasa recta, as medullar interstitium is less and less concentrated as we go up to the cortex, water is reapsorbed (osmosis) and ions (NaCl) are lost (passive diffusion down their concentration gradient from vasa recta to medulla). So, at the end of ascending part of vasa recta osmolarity should be the same as at the beginning which means 300 mOsm/l, but it isn't 300, it is slightly higher - about 320 mOm/l.
    Of course, don't believe me too much. Maybe I have made some mistakes, I can't say for sure.

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    Just to correct myself, urine can have osmolarity between 50 and 1200 mOsm/l. Why 50 mOsm when we know that at the end of ascending part of loop of Henle osmolarity is 100 mOsm/l? Because, when there is no ADH, then, in DCT NaCl is still reapsorbed and water isn't, so tubular osmolarity decreases a little from 100 to 50 mOsm/l.

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    Petarm. Thank you so much. I can finally now undertand the relationship of what would happen if electrolytes were not being absorbed (less than 2/3 )in the PCT. This forum rocks!!!

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