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In renal physiology, reabsorption, more specifically tubular reabsorption, is the process by which the nephron removes water and solutes from the tubular fluid (pre-urine) and returns them to the circulating blood.[1] It is called reabsorption (and not absorption) because these substances have already been absorbed once (particularly in the intestines) and the body is reclaiming them from a postglomerular fluid stream that is on its way to becoming urine (that is, they will soon be lost to the urine unless they are reabsorbed from the tubule into the peritubular capillaries. This happens as a result of sodium transport from the lumen into the blood by the Na+/K+ATPase in the basolateral membrane of the epithelial cells. Thus, the glomerular filtrate becomes more concentrated, which is one of the steps in forming urine. Nephrons are divided into five segments, with different segments responsible for reabsorbing different substances.[2] Reabsorption allows many useful solutes (primarily glucose and amino acids), salts and water that have passed through Bowman's capsule, to return to the circulation. These solutes are reabsorbed isotonically, in that the osmotic potential of the fluid leaving the proximal convoluted tubule is the same as that of the initial glomerular filtrate. However, glucose, amino acids, inorganic phosphate, and some other solutes are reabsorbed via secondary active transport through cotransport channels driven by the sodium gradient.
The bladder is able to separately reabsorb water and solutes such as drugs.[3] This mechanism is not affected by anticholingeric drugs, unlike renal reabsorption.[4] This mechanism also does not involve arginine vasopressin.[5] In fully hydrated frogs, the bladder plays a significant role in reabsorbing water and electrolytes.[6] The pig urothelium expresses AQP3, AQP9, and AQP11.[7]