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Proximal Convoluted Tubule
Proximal Convoluted Tubule
The proximal convoluted tubule avidly reabsorbs filtered glucose into the peritubular capillaries so that it is all reabsorbed by the end of the proximal tubule.
From: Quantitative Human Physiology, 2012
CreatinineUreterNephronParathyroid HormoneDistal Convoluted TubuleNephrosisLoop of HenleRenal PelvisReabsorptionVitamin D
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J.M. Sands, J.W. Verlander, in Comprehensive Toxicology, 2010
The PCT is responsible for reabsorbing 50–60% of the glomerular ultrafiltrate. Thus, it is a site for high volume reabsorption, but not for regulation of the final composition of the urine. The latter task is the responsibility of the collecting duct.
The PCT reabsorbs solute isosmotically. Water is reabsorbed through the aquaporin-1 (AQP1) water channel (Nielsen et al. 1993b; Preston et al. 1992) located in both the apical and basolateral plasma membranes. Water reabsorption is driven by reabsorption of NaCl and NaHCO3. NaCl and NaHCO3 are transported via a variety of transcellular and paracellular mechanisms, including sodium–proton antiporters (NHE3), sodium–bicarbonate cotransporters (NBC), and a chloride–formate antiporter (CFEX). Under normal conditions, most of the filtered bicarbonate is reabsorbed.
The PCT is responsible for reabsorbing most of the glucose, amino acids, and small peptides that enter the ultrafiltrate (Berry and Rector 1991). The PCT contains numerous secondary active, sodium-coupled transporters for glucose (SGLT2) and amino acids (Silbernagl and Gekle 2008; Silverman 2008). Many of these transport proteins have been cloned and several isoforms of each transporter have been identified (Silbernagl and Gekle 2008; Silverman 2008). These sodium-coupled cotransporters all take advantage of the low intracellular sodium concentration, generated by the Na+/K+-ATPase pump, to drive transport. Thus, the PCT has a high metabolic demand and is particularly sensitive to anoxic injury. Damage to the PCT results in Fanconi’s syndrome with glucosuria, aminoaciduria, and a proximal renal tubular acidosis.
The PCT transports or metabolizes many drugs and toxicants. It secretes organic acids, is the predominant site of renal cytochrome P450, and has several multidrug resistance proteins (MRP1–5) (Berry and Rector 1991; Burckhardt and Koepsell 2008; Hennessy and Spiers 2007; Kartner and Ling 1989). Secretion of organic anions, such as p-aminohippurate (PAH), occurs by sodium-dependent secondary active transport from peritubular capillaries into the PCT cell across the basolateral plasma membrane. There are several organic anion transporters (OAT) in the basolateral membrane, including OAT4, OATv1, OATPA, OAT-K1, and OAT-K2 (Burckhardt and Koepsell 2008; Koepsell et al. 2007). There are also several organic anion transporters in apical membrane secretory pathways, including OAT1, OAT2, and OAT3 (Burckhardt and Koepsell 2008; Koepsell et al. 2007). The PCT is the major source of renal cytochrome P450 (Badr 1995).
Organic cations are also secreted by sodium-dependent secondary active transport. In general, organic cations enter the cell across the basolateral plasma membrane by a facilitated transport pathway, organic cation transporter1–3 (OCT1-3) (Burckhardt and Koepsell 2008; Dantzler 2003). They are secreted into the tubule lumen by an amiloride-inhibitable NHE3 coupled to a protein–organic cation exchanger with the net result being sodium–organic cation exchange (Burckhardt and Koepsell 2008; Dantzler 2003). Many of these transport proteins have been cloned and several isoforms of each transporter have been identified (Burckhardt and Koepsell 2008; Dantzler 2003). A second apical secretory mechanism is an organic cation ATPase (Pritchard 1995). Many pharmaceuticals and toxicants are organic cations or anions that are carried by these transporters, thereby rendering the PCT very sensitive to damage by drugs and toxicants.
Peptides and proteins smaller than albumin can enter the ultrafiltrate across the glomerulus (Johnson and Maack 1995), and small proteins can be reabsorbed by nonspecific endocytotic reabsorption. Peptides are reabsorbed by sodium-coupled secondary active transport pathways (Silbernagl and Gekle 2008). Many small peptides are taken up by PCT cells, including insulin, glucagon, and other peptide hormones. The PCT cells degrade these small peptides and albumin in lysosomal vacuoles, which contain proteases such as cathepsins. Cathepsins B and L are found in highest abundance in the PCT, but are also found in the PST (Olbricht et al. 1986). When GFR is reduced, as during renal insufficiency, the serum half-lives of these peptide hormones are increased because their filtration and subsequent degradation by the PCT is reduced.
Finally, the PCT reabsorbs divalent cations. Calcium is reabsorbed isosmotically in parallel with sodium. Magnesium is also reabsorbed passively but is less permeant than calcium. Magnesium must achieve a tubular fluid to plasma ratio of 1.5 before it is reabsorbed (Quamme and Dirks 1980).
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Mechanism of Concentration and Dilution of Urine
Joseph Feher, in Quantitative Human Physiology (Second Edition), 2017
Increased Solute Loads in the Distal Nephron Produce an Osmotic Diuresis
The proximal convoluted tubule avidly reabsorbs filtered glucose into the peritubular capillaries so that it is all reabsorbed by the end of the proximal tubule. The mechanism for glucose reabsorption was described in Chapter 7.4. The proximal tubule is the only site for glucose reabsorption. If the filtered load of glucose overwhelms the proximal tubule transport mechanisms, glucose escapes to the loop of Henle. There is no reabsorption of glucose beyond the proximal tubule, and the glucose becomes progressively more concentrated as the nephron reabsorbs water and salt. The glucose exerts an osmotic pressure and produces an osmotic diuresis, the severity being directly proportional to the amount of excreted glucose. This is the origin of the polyuria of persons with uncontrolled diabetes mellitus in which the plasma concentration of glucose exceeds its renal threshold. Any osmotically active material in the distal nephron will have this effect. Mannitol is freely filtered by the kidney but neither secreted nor reabsorbed. Injection of mannitol will produce an osmotic diuresis that is directly proportional to the amount of mannitol injected.
Which of the following would not be reabsorbed (removed from the filtrate and returned to the blood) at the proximal convoluted tubule? A) Glucose. B) Creatinine. C) Urea. D) Bicarbonate.
Answer to: Which of the following would not be reabsorbed (removed from the filtrate and returned to the blood) at the proximal convoluted tubule?...
Which of the following would not be reabsorbed (removed from the filtrate and returned to the...
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Which of the following would not be reabsorbed (removed from the filtrate and returned to the blood) at the proximal convoluted tubule?
A) Glucose. B) Creatinine. C) Urea. D) Bicarbonate.
The Kidney and Reabsorption:
The kidney is responsible for four main processes: filtration, reabsorption, secretion, and excretion. The reabsorption process is where certain products are returned to the blood after the filtration process if they are still needed by the body.
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The answer is B) Creatinine. Creatinine is considered a waste product, which is why it would not be reabsorbed; it would be secreted and then excreted...
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The Three Processes of Urine Formation
Chapter 3 / Lesson 13
Understand the process of urine formation and review the urinary system. Examine where steps like filtration occur and know how they operate within urine production.
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Tubular reabsorption article (article)
Tubular reabsorption article
What is tubular reabsorption?
The fluid that filters through the glomerulus and Bowman’s capsule (glomerular filtrate) is very similar to blood plasma without the proteins, and at this point not at all like urine. If this filtrate flowed straight to your bladder and then out your body, you would lose more than 10-times the entire volume of your extracellular body fluids (plasma and interstitial fluid) every day. Fortunately, tubular reabsorption mechanisms in the nephrons of your kidneys return the water and solutes that you need back into your extracellular fluid and circulatory system. In addition to reabsorbing the substances that you need, your nephrons are able to secrete unwanted substances from your bloodstream into the filtrate. Together these processes complete the transformation of the glomerular filtrate into urine.
Tubular reabsorption is the process that moves solutes and water out of the filtrate and back into your bloodstream. This process is known as reabsorption, because this is the second time they have been absorbed; the first time being when they were absorbed into the bloodstream from the digestive tract after a meal.
How does reabsorption in the nephrons work?
The nephrons in your kidneys are specifically designed to maintain body fluid homeostasis. This means keeping extracellular body fluid volumes stable, as well as maintaining the right levels of the salts and minerals that are essential for the normal function of your tissues and organs; regardless of how much you eat, or how active you are. Nephrons are divided into five segments, with different segments responsible for reabsorbing different substances.
Overview of the nephron showing which substances get reabsorbed along the various structures of the nephron (like the proximal convoluted tubule).
Reabsorption is a two-step process:
The first step is the passive or active movement of water and dissolved substances from the fluid inside the tubule through the tubule wall into the space outside.
The second step is for water and these substances to move through the capillary walls back into your bloodstream, again, either by passive or active transport.
Nephrons are comprised of different segments that perform specific functions. The walls of the nephron are made of a single layer of cube-like cells, called cuboidal epithelial cells, and their ultrastructure changes depending on the function of the segment they are in. For example, the surface of the cells facing the lumen of the proximal convoluted tubule are covered in microvilli (tiny finger-like structures). This type of surface is called a brush border. The brush border and the extensive length of the proximal tubule dramatically increase the surface area available for reabsorption of substances into the blood enabling around 80% of the glomerular filtrate to be reabsorbed in this segment. Another notable feature of these cells is that they are densely packed with mitochondria (the cell’s energy generators). The mitochondria ensure a good supply of energy is available to fuel the active transport systems needed for efficient reabsorption.
Diagram showing what a proximal tubule epithelial cell looks like.
Passive transport is when substances use specific transporters to move down their concentration gradient (from areas of high concentration to areas of low concentration) or in the case of charged ions, down their electrochemical gradient.
Active transport is when substances are moved up (or against) their concentration or electrochemical gradients (from low to high). In this case, the substances are transported back into the bloodstream via energy-dependent, or active transport proteins.
Reabsorption of sodium, nutrients, water, and other ions
Sodium is the major positively charged electrolyte in extracellular body fluid. The amount of sodium in the fluid influences its volume, which in turn determines blood volume and blood pressure. Most of the solute reabsorbed in the proximal tubule is in the form of sodium bicarbonate and sodium chloride, and about 70% of the sodium reabsorption occurs here. Sodium reabsorption is tightly coupled to passive water reabsorption, meaning when sodium moves, water follows. The movement of water balances the osmotic pressure within or across the tubule walls, which maintains extracellular body fluid volume.
Reabsorption in the early proximal convoluted tubule: The most essential substances in the filtrate are reabsorbed in the first half of the proximal convoluted tubule (early proximal tubule). These include glucose, amino acids, phosphate, lactate and citrate, which “piggy-back” on sodium co-transporters (membrane proteins that link the movement of two or more specific solutes together) that move sodium down its electrochemical gradient into tubule epithelial cells. For this to continue, the sodium gradient must be maintained, which means sodium cannot be allowed to build up inside the epithelial cells of the proximal tubule wall. This is achieved using:
Sodium/potassium ATPase, a sodium pump (active transporter) located on the opposite side of the epithelial cell that takes care of this by moving three sodium ions out of the cell for reabsorption into the bloodstream, and pumping two potassium ions back into the cell (see diagram below).