Renal Tubular Reabsorption and Secretion PDF

the tubular membrane. A large part of this water flow occurs through aquaporins in the cell membranes, as well as tight junctions between epithelial cells. In more distal parts of the nephron. Beginning in the loop of Hennelly, the tight junctions become far less permeable to water so that water can...

the tubular membrane. A large part of this water flow occurs through aquaporins in the cell membranes, as well as tight junctions between epithelial cells. In more distal parts of the nephron. Beginning in the loop of Hennelly, the tight junctions become far less permeable to water so that water can not move as easily. However, antidiuretic hormone or ADHD greatly increases the water permeability in the distal and collecting tubules. So in summary, the in the proximal tubule and the descending loop of Hindley. Water permeability is always high due to the bonded expression of aqua and one water channels in the ascending loop of Hindley, water permeability is always low, so there's almost no water reabsorption. And in the distal tubules, collecting tubules and collecting ducts. Water permeability is caused by aquaporins that are dependent upon the presence of ADHD. When sodium is reabsorbed from the tubular lumen. Negative ions such as chloride are transported along with the sodium. Because of electrical potentials, sodium movement leaves the inside of the lumen negatively charged, causing chloride to diffuse passively through the cellular pathway. As sodium and water are reabsorbed from the tubular lumen, the chloride ions are concentrated, causing a concentrated gradient to develop in passive diffusion to occur. Thus, the active reabsorption of sodium is closely coupled to the passive reabsorption of chloride caused by the electrical potential and the chloride concentration gradient. Chloride ions are also reabsorbed by secondary active transport across the luminal membrane. Urea is also passively reabsorbed from the tubule, but to a much lesser extent than chloride as water is reabsorbed from the tubules. Concentration increases and a concentration gradient gradient favoring reabsorption occurs. However, the tubule is not easily permeable to urea, so that only about half of the filtered urea is reabsorbed by the tubules. The remaining 50% passes into the urine, allowing for large amounts to be excreted. Another waste product of metabolism is creatinine. The tubular membrane is essentially impermeable to it because it is a large molecule, and therefore none of the creating that is filtered is reabsorbed, and virtually all is excreted in the urine. 65% of the filtered sodium and water are reabsorbed in the proximal tubule. This high capacity results from its special cellular characteristics. The proximal tubule has a large number of mitochondria to provide energy and support powerful active transport processes. It also has a large brush border on the luminal side of the membrane, and extensive channels on the basal or side that together provide an extensive surface area on both sides of the epithelial cell for rapid transport of sodium and other substances. There is extensive protein carrier molecules for Co transport mechanisms of sodium, along with other organic nutrients, as well as counter transport mechanisms for the secretion of hydrogen ions. The sodium potassium pump provides the major force for reabsorption of sodium chloride and water. Much of the glucose, amino acids, and other solutes are absorbed by Co transportation during the first half of the proximal tubule. Higher and higher concentrations of chloride in the second half are then absorbed. The amount of sodium in the tubular fluid decreases. The concentration remains the same because water permeability is so great. Water is absorbed at the same rate as sodium. Glucose, amino acids and bicarbonate are avidly reabsorbed, and their concentrations decrease markedly in the proximal tubule. Solutes such as creatinine increase in concentration, making the osmolarity remain the same. Organic acids and bases such as bile salts, oxalate, urate, and catecholamines are also excreted uh in the proximal tubule. In addition to the waste products of metabolism, harmful drugs and toxins are excreted in tubules as well as para amino acid. Uh para amino hipp uric acid is cleared so rapidly that it can be used to estimate renal plasma flow. The loop of Henley consists of three functionally different segments the thin descending, the thin ascending, and the thick ascending. The thin descending and thin ascending have thin epithelial membranes with no brush border. Few mitochondria and low levels of metabolic activity. The function of the thin descending is to allow for simple diffusion. It is highly permeable to water and moderately permeable, permeable to most solids. 20% of the filtered water is reabsorbed in the loop of Henley. Almost all of it in the thin descending limb. Both portions of the ascending limb are impermeable to water, which is important for concentrating urine. The thick epithelial cells of the ascending limb have high metabolic activity and are capable of active sodium chloride and potassium reabsorption. An important component for reabsorption in the thick of sending limb is a sodium potassium ATP pump in the epithelial cell basal outer membrane. So this guy here. The reabsorption of solutes in the segment is closely linked to the capability of this pump to maintain the low intracellular sodium concentration. So low sodium intracellular. Um. Which of course, this provides the favorable gradient for the movement of sodium from the tubular fluid into the cell. Uh, this this provides the gradient for the secondary active transport of the one sodium two chloride one potassium transporter in the thick ascending. So this person, this, uh, transporter. There's also a sodium hydrogen counter transporter for sodium reabsorption and hydrogen secretion. The reabsorption of magnesium, calcium, potassium, and more. Sodium is caused by the slightly positive charge of the tubular lumen. So you see here the positive charge of the tubular and driving positively charged. Um. Salutes through and out. Uh, the thick segment of the ascending loop is virtually impermeable to water. And therefore, by absorbing these solutes, uh, the water becomes very dilute. This is important for diluting and concentrating properties of the kidney. This decisive action for loop diuretics, which inhibit the sodium potassium two chloride transporter. So you can see on the slide here it says Lasix, um, is inhibiting this transporter. First portion of the distal tubule forms the macula denser, that is part of the juxtaposed Mary-Lou complex, which provides feedback and control of GFR and blood flow. Uh, that we've talked about before. The distal tubule was referred to as the diluting segment because it also absorbed sodium potassium chloride, but is virtually impermeable to water and urea. The thighs I diabetics inhibit the sodium chloride cotransporter here. The second half of the distal tubule and cortical collecting ducts has similar functional characteristics. They're composed of principal cells which reabsorb sodium and water and secrete potassium, and intercalated cells, which reabsorb potassium and secrete hydrogen into the tubular lumen. We'll cover those cells more thoroughly. Coming up. The principal cells perform sodium reabsorption and potassium secretion that is dependent upon the activity of the sodium potassium pump in the basal lateral membrane. So once again, the sodium potassium pump in the basal latter membrane uh. This causes potassium to be pumped into the cell. Uh, and it maintains a high intracellular potassium concentration. This potassium then diffuses down its concentration gradient into the tubular lumen. Is the primary site of action of potassium sparing diuretics and sodium channel blockers. The sodium channel blockers inhibit the entry of sodium into the tubular cells. Uh, here, as you can see with the sign, um. Which reduces the activity of the sodium potassium pump that then decreases the transport of potassium into the cell. It reduces the secretion of potassium into the tubular fluid. The intercalated cells make up 30 to 40% of the cells in the collecting tubules and collecting ducks. They play a major role in acid base regulation. There are two types. Type A secretes hydrogen using a hydrogen ATP pump and hydrogen potassium ATP transporter. Type B has the opposite function of the type A, uh. Type B secretes bicarbonate ions into the tubule lumen and reabsorb hydrogen. Type A is to correct acidosis. Type B is to correct alkalosis. Both types of cells utilize carbonic anhydrase to make hydrogen and bicarbonate intracellular. The chloride bicarbonate powder transporter on the apical membrane is called pinion. So this pinion transporter comes up later when chronic metabolic alkalosis is present. The number of type B intercalated cells increases when there's chronic acidosis. Type A cells increase. The functional summary of the late distal tubule and cortical collecting tubule. Uh, are these things? Um, one it's impermeable to urea. Both portions reabsorb sodium, primarily controlled by aldosterone, and also secrete potassium. Type A, intercalated cells actively secrete hydrogen, and type B intercalated cells secrete bicarbonate. The permeability of the late tubule and cortical collecting ducts to water is controlled by 80 or vasopressin. The Magellanic collecting ducts reabsorb less than 5% of the filtered water and sodium. But they are the final site for processing urine and therefore play critical role in determining the final output of water and solids. The cells are nearly cuboid, all in shape, with smooth surfaces that lack the brush border, while they also have very few mitochondria. Permeability of water is controlled by antidiuretic hormone with high levels. Water's water is avidly reabsorbed, which of course reduces urine volume and concentrates it. There are special urea transporters to facilitate diffusion, tubular cells, and eventually the paired tubular capillary. This raises the osmolality and increases the kidney's ability to form concentrated urine. Lastly, the Magellanic collecting duct secretes hydrogen ions against a large concentration gradient. Whether solutes become concentrated is determined by the relative degree of reabsorption of that solute versus the reabsorption of water. The changes in concentration are represented in this graph. As the filtrate moves along the tubular system. Concentrations rise higher if more water is reabsorbed than solute, or fall. If more solute is reabsorbed than water, you can see substances such as creatinine and urea become highly concentrated in the urine. So Korea and Korea you can see their concentrations raise. These substances are not needed by the body, and the kidneys have become adapted to minimally reabsorb them or even secrete them. Other substances, such as glucose and amino acids at the bottom. Uh, obviously glucose and amino acids here. Um. Are strongly reabsorbed because they are needed by the body. You can see the substances inulin in the graph as well. So there's inulin. Um, inulin is used to measure GFR. It is not reabsorbed or secreted by renal tubules. So changes in concentration reflect changes in water reabsorption at the end of the proximal tubule. You can see the inulin ratios around three proximal tubule in. So ratios around three. Uh, this means that the concentration is three times greater than when it was filtered, meaning only one third of the filtered water remains and two third has two thirds has been reabsorbed. It is essential to maintain a precise balance between tubular absorption and glomerular filtration. There are multiple nervous, hormonal, and local control mechanisms that regulate this. An important feature is some solutes can be regulated independently of others, especially through hormonal control. We will now go go over each of these specifically. To marry. The tubular balance refers to the phenomenon of increased reabsorption rate in response to increased tubular load or inflow. For example, if GFR increases from 125 to 150ml a minute, proximal tubular reabsorption also increases from 81ml a minute to 97.5. Or about 65% of GFR. So. Percentage remains the same. So percentage times of filtrate increases reabsorption. The rate of reabsorption increases as the filtered load increases and the percentage of reabsorption remains is the same constant. Some degree of reabsorption is increased in other tubular segments, but the precise mechanism is not fully understood. This can occur independent of hormones as it can be demonstrated in isolated kidneys. The skull. Mario tubular balance helps prevent overloading of the distal tubular segments when GFR increases. Combined with renal auto regulatory mechanisms, especially the tubular glomerular feedback, these prevent large changes in fluid flow in the distal tubules when arterial pressure or sodium balance changes. Okay. So there's a lot in this slide. So let's go through it slowly. Hydrostatic and colloid osmotic forces govern the rate of reabsorption across the peri tubular capillaries, just as they do with the glomerular capillaries. Uh, more than 99% of the water, and most of the solutes are absorbed from the filtrate as it passes through the renal tubules. The normal rate of tubular capillary reabsorption is 124mm a minute. Of course, this is subject to the hydrostatic and colloid forces that we have discussed before. Net filtration pressure equals capillary pressure minus interstitial hydrostatic pressure minus capillary colloid pressure minus interstitial fluid. Colloid pressure. In this instance we're subtracting the colloid pressure to show the