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The loop of Henle has evolved because osmosis consumes and produces dioxygen, O2, and the looped thin segment allows the O2 produced within the thin descending limb during exosmosis, to recirculate out of the thin ascending limb and into the vasa recta, that flows in the opposite direction to the filtrate to return the O2 to the ascending vasa recta. The pump  that generates osmotic transfer of water, is the phase that water forms as it is forced into a solid phase when it contacts surfaces. This surface phase  is charge polarized, because the hydrogen ions that separate the lattice sheets in the ice phase of water have been squeezed out , to make it more dense than water (the only way a phase change from pressure against surfaces is favourable), and the excluded hydrogen ions protonate water on top of this solid phase. Traditional osmosis is a result of asymmetry in this phase on either side of a membrane, from that the solid phase of water is impaired by solutes. But that is not the only way this pump  can generate osmosis. In a narrow tube, the positively charged surface of this phase will repel across the diameter of the tube, pushing protons across the tube wall, causing the negatively charged (H3O2-)n phase to break down into electrons, that transfer across the wall as well, and O2, while the protons and electrons combine with O2 on the outside of the tube to form water. This osmosis effect in narrow tubes is the physiological basis for the kidney. It removes water from the filtrate (via the ascending vasa recta that drains into the interlobular artery), and dehydrates the medulla. The reason the narrow tube has formed a loop, is that a straight tube that drained into the papilla would also lose all the O2 that was produced in the osmotic pump  mechanism. But a tube that loops, could return the O2 to be used again, by reversing the osmosis. The kidney evolved the loop of Henle to do exactly that, and it has oriented the vasa recta in the opposite flow direction specifically to recirculate the O2. The recirculation of O2, is in a 1:2 relationship with another recirculation system, the H2O that is transferred osmotically to consume O2 at the thin ascending limb. This water recirculates from the collecting duct, and into the thin ascending limb. It dilutes the filtrate as it travels from the bend of the loop of Henle and into the collecting duct, but is then reabsorbed, leaving the filtrate isotonic with what it was at the bend of the loop of Henle. It is there only to maintain the recirculation of the O2. The result is the same as if a straight tube that drained into the papilla received infinite O2. To support the endosmosis at the thin ascending limb that transfers the O2 in the loop of Henle back into the vasa recta, this segment has evolved a lumen diameter that is gradually increasing, all the way from the bend of the loop of Henle up to the thick ascending limb. Any surplus water, besides that necessary to recirculate the O2, is prevented from entering the medulla, by the low blood supply to the medulla that the kidney evolved to avoid adding any water after the desalination takes place at the thin descending limb. The kidney is able to increase or decrease the desalination effect at the thin descending limb, by regulating filtration pressure. Less pressure means less water is forced into the surface phase , and a weaker repelling force across the lumen. The kidney has evolved so that the filtration pressure is strongest in the tubes that supply the largest surface area, the juxtamedullary nephrons with long loops that reach the inner medulla. It supplies these glomeruli with more proximal branches from the interlobular artery. The recirculation of water is regulated by the resistance to flow in the collecting duct tree, and, the permeability to water in the collecting duct epithelia. The hormone vasopressin, secreted by the posterior lobe of the pituitary gland, regulates both of these. It contracts fibroblasts in the medulla, shrinking the diameter of the collecting duct, and, it upregulates aquaporin channels in the epithelial cells. Kidney function has to be maintained even as systemic pressure, cardiac output, changes with different activities, such as at rest or during physically demanding activity. It has evolved a reflex to do exactly this, tubuloglomerular feedback at the juxtaglomerular apparatus. It is able to maintain filtration pressure even as systemic pressure changes. This ensures that the desalination mechanism at the thin descending limb, is proportional to the recirculation of water, i.e., that the kidney does what the hypothalamus tells it to do (via vasopressin, the antidiuretic hormone) regardless of if the body is at rest or not.
"The purpose of the counter-current system in the loop of Henle is to reabsorb the O2 that is produced in the thin descending limb during the osmotic  reabsorption of water there, that is how and where the kidney desalinates water and reabsorbs it into the renal vein. Without the loop, the O2 trapped in the nephron would just pass straight out into the urine, allowing only a one-time use of the osmosis cathode O2. If the body absorbs 22 mol O2 per day, and 1/5th of that passes into the kidney, there is only 4.4 mol O2 in the kidney, and if all of it were used for the desalination mechanism, without recirculation, it could only reabsorb 2*4.4 mol water, equal to 8.8/55.5 = 15 dL, far from the 10 L/d of water that is removed with the thin descending limb of the loop of Henle. The counter-current loop, and the vasa recta flowing in the opposite direction, allows the O2 to recirculate, and using 4.4 mol O2 as an example again, recirculating 63 times provides the osmotic cathode to reabsorb 10 liters of water per day, 63*8.8 mol / 55.5 mol/L = 10 L. "
The pressure from glomerular filtration pushing water into the thin descending limb, and against the epithelium in it, is generating a charge polarized phase of water against the surface, that is positively charged towards the lumen, causing it to repel itself, and pump protons and electrons across the thin epithelium (while producing dioxygen), that recombine with dioxygen in the ascending vasa recta to produce water, that is transported out into the interlobular vein. This makes the filtrate that passes into the medulla and through the bend of the loop of Henle hypertonic, allowing water to transport from the collecting duct into the thin ascending limb, osmotically, aided by the continuous lumen diameter increase in the thin ascending segment, and the dioxygen produced in the thin descending limb. The generation of an "osmotic" removal of water from the thin descending limb, generated by "diametric repulsion" on the surface phase of water, is the physiological basis of the kidney. It is maintained by the juxtaglomerular apparatus, where macula densa cells at the distal convoluted tubule sense the osmolarity of the filtrate, the balance between water removal at the thin descending limb, and water transfer from the collecting duct into the thin ascending limb, and increase glomerular filtration pressure by release of renin that constricts the efferent arteriole, as well as activates systemic endocrine systems that increase pressure in the renal artery. The pressure from the heart is prioritized for juxtamedullary nephrons, that are supplied by more proximal branches from the interlobular artery, and has loops of Henle that dive deep into the medulla, and cortical nephrons receive lower pressure, and have lower glomerular filtration pressure.
Aquatic organisms are bathed in water. In the same way water is pulled with particles when excreted from the kidney, water is pulled into the organism when its osmolarity increases as amino acids are degraded into HCO3- and NH4+. To the aquatic organism, there is no water cost to excrete these byproducts, water will first flow inwards to neutralize the osmotic balance, and then follow along outwards for the same reason. The terrestrial organism on the other hand will not have the inwards osmotic equilibration that aquatic organisms have. To the terrestrial organism, the byproducts from amino acid catabolism have a large cost in water. This is the reason terrestrial organisms have evolved ways to lower that cost, by turning the HCO3- and NH4+ into CO2 and urea. Urea is a weaker base than ammonia, and will free the proton on NH4+ to combine with HCO3-, forming carbon dioxide that can be exhaled with no water cost, removing 50% of the cost. Urea also combines two NH3 into a single molecule, lowering the osmotic pressure by 2x, reducing the total osmotic cost with another 25%. The end result is that only 1/4th as much water is needed.
Loop of Henle thin segment generates passive single effect in kidney The idea is simple. The thin segment  in the metanephros (the one terrestrial animals have) is homologous to thin segment  in mesonephros (that aquatic animals have) and archinephros (that is a bit evolutionarily older than mesonephros). Homer Smith, the world leading authority on kidney in early 1900s, detailed this in his original work from 1935. In mesonephros it has formed a loop that dives deep into kidney towards the papilla  where urine eventually drains. This loop  was discovered in 1800s by a Jacob Henle and is named after him, Henle s loop . Since it is thin , resistance to fluid flowing into it is high. This forces the fluid to concentrate itself. That is self-evident based on standard fluid dynamics. This is what people have missed. It is a passive  effect for the countercurrent multiplication. Such a mechanism has been theorized for 50 years, but, so, it is self-evident that this is what causes it. It is powered by pressure from the heart, the kidney in mammals receives 1/5th of cardiac pressure (arms, head, legs, and stomach organs get the other 4/5ths. ) This passive  mechanism is then monitored by the main function-monitoring-system of the kidney, the juxtaglomerular apparatus . People think it is monitoring blood pressure  basically. Like, as if animals have trouble with that. Synapses Smith, H. W., Thomson, K. S., Little, Brown and Company,, & McClelland and Stewart Limited,. (1953). From fish to philosopher. Boston: Little, Brown and Company. Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97 Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008 Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018 Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010 Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2
The glomerular filtration reflex in the juxtaglomerular apparatus is likely monitoring the passive single effect Kokko & Rector alluded to in 1972 (Kokko, 1972; Sands, 2009). This passive osmotic multiplier is generated by the resistance peak at the thin segment that Mark Knepper has documented (Knepper, 2018), and that is self-evident based on standard fluid dynamics. Harold Layton alluded to the passive osmotic multiplier as well (Layton, 2011), and he also referenced Berliner who also alluded to the same mechanism (Berliner, 1958). Synapses Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97 Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008 Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018 Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010 Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2
The glomerular filtration reflex in the juxtaglomerular apparatus is likely monitoring the passive single effect Kokko & Rector alluded to in 1972 (Kokko, 1972; Sands, 2009). This passive osmotic multiplier is generated by the resistance peak at the thin segment that Mark Knepper has documented (Knepper, 2018), and that is self-evident based on standard fluid dynamics. Harold Layton alluded to the passive osmotic multiplier as well (Layton, 2011), and he also referenced Berliner who also alluded to the same mechanism (Berliner, 1958). Synapses Kokko, J. P., & Rector, F. C., Jr. (1972). Countercurrent multiplication system without active transport in inner medulla. Kidney International, 2(4), 214 223. https://doi.org/10.1038/ki.1972.97 Sands, J. M., & Layton, H. E. (2009). The Physiology of Urinary Concentration: An Update. Seminars in Nephrology, 29(3), 178 195. https://doi.org/10.1016/j.semnephrol.2009.03.008 Gilmer, G. G., Deshpande, V. G., Chou, C.-L., & Knepper, M. (2018). Flow resistance along the rat renal tubule. American Journal of Physiology-Renal Physiology, 315(5), F1398 F1405. https://doi.org/10.1152/ajprenal.00219.2018 Layton, A. T., & Layton, H. E. (2011). Countercurrent multiplication may not explain the axial osmolality gradient in the outer medulla of the rat kidney. American Journal of Physiology-Renal Physiology, 301(5), F1047 F1056. https://doi.org/10.1152/ajprenal.00620.2010 Berliner, R. W., Levinsky, N. G., Davidson, D. G., & Eden, M. (1958). Dilution and concentration of the urine and the action of antidiuretic hormone. The American Journal of Medicine, 24(5), 730 744. https://doi.org/10.1016/0002-9343(58)90377-2