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Bavidra Why and how does the kidney change urine osmolarity? How do diuretics affect this process?
The kidney changes urine osmolarity by controlling the amount of water excreted in the urine. This is essential as it determines the osmolarity of the extracellular fluid which controls the amount of water that moves in and out of the cell through osmosis. In conditions of abnormally high water intake, the kidney adapts into a diuretic state and a large volume of dilute hypotonic urine is excreted. This is to prevent the extracellular fluid becoming hypotonic which would result in water osmosing into the cell and in extreme cases can lead to the cell bursting. But in conditions of excessive water loss through sweating or low water intake, kidney becomes anti-diuretic and water is conserved through excretion of a small volume of concentrated hypertonic urine. The switch between these two states is mediated by ADH which is a hormone released from the posterior pituitary in conditions of hydropenia. Under average conditions, 1500ml of urine with an osmolarity of 600mOsmol is excreted. The first stage of water reabsorption occurs in the proximal tubule where 2/3rd of the water in the ultrafiltrate is reabsorbed isotonically. This occurs as the proximal tubule has a high water permeability due the prescence of large number of aquaporins in the apical and basolateral membranes of the leaky epithelial cells. As a result of this, the reabsorption of solute, which is often coupled to Na+ is followed by water. Counter current exchange system The next stage of water reabsorption occurs in the loop of Henle, where a counter current exchange system reabsorbs salt in excess of water and creates a hypertonic interstitium in the renal medulla and hypotonic urine which then enters the collecting duct. The first step of the multiplier system is known as the single effect and occurs in the thick ascending limb which is impermeable to water. It involves the transport of NaCl from the lumen into the epithelial cells by the apical, electroneutral Na/K/Cl cotransporter which couples the influx of 1Na+, 1K+ and 2Cl-. This transport is powered by the Na+ gradient created by the basolateral Na/K pump which uses the energy from the hydrolysis of ATP to couple the transport of 3Na+ out of the cell and 2K+ into the cell, both against the gradient . The Na then enters the interstitium through the Na/K pump, whereas the Cl- enters through chloride ion channels. Additional to this, there is also a small amount of Na+ that enters the interstitium through the tight junctions and is driven by the transepithelial positive voltage. As a result of these processes there is a net movement of NaCl into the interstitium which causes it to become hyperosmolar. Following the creation of a hyperosmolar interstitium, the ultrafiltrate in the descending limb instantaneously equilibriates with the lumen of the descending
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