Renal Tubular Reabsorption and Secretion PDF

net reabsorption pressure. So let's go through that a little bit more. So reabsorption equals the filtration coefficient times the net forces and the net forces. Equal these. So the capillary pressure, the hydrostatic pressure which is here minus the interstitial hydrostatic pressure. Um. And then t...

net reabsorption pressure. So let's go through that a little bit more. So reabsorption equals the filtration coefficient times the net forces and the net forces. Equal these. So the capillary pressure, the hydrostatic pressure which is here minus the interstitial hydrostatic pressure. Um. And then the capillary osmotic pressure minus the interstitial osmotic pressure. So, uh, if we said the capillary pressure is 13 minus the interstitial pressure pushing uh into the capillary is six. So those forces are opposing each other. Uh, that leaves us seven. Um. And balance. And that's a seven in the. For filtration, uh, in the direction of excretion. And then we have osmotic pressures. Uh, 32 for the capillary osmotic pressure and a 15 for the interstitial osmotic pressure. So of course you subtract those and you have the balance of 17. And that's 17 in the reabsorption direction. So we have a net reabsorption of ten. Uh, this reabsorption is then multiplied times the, uh, filtration coefficient. And given your overall reabsorption. So the high there is a high filtration coefficient. And that's due to the high hydraulic conductivity and large surface area of the capillaries. And once again hydrostatic pressure, colloid osmotic forces and the large filtration coefficient. The two determinants of period tubular capillary reabsorption, directly influenced by renal hemodynamic changes of the hydrostatic and colloid osmotic pressures. Within the capillaries, arterial pressure raises peri tubular capillary hydrostatic pressure and decreases reabsorption. Increase pressure, uh increases the pressure and the uh outward pressure decreases reabsorption. So smaller reabsorption, uh, an increase in resistance in the afferent or efficient arterials reduces. So if you had increased resistance and after and after and arterials reduced pressure, uh, period to the capillary hydrostatic pressure and increased reabsorption. Um, raising the colloid osmotic pressure increases peri tubular capillary absorption. So if you increase this, you increase this, um, the systemic plasma colloid osmotic pressure raises the tubular capillary colloid osmotic pressure, thereby increasing reabsorption. Of course this is done by raising the plasma protein concentration of the systemic blood. Uh, next, the higher the filtration fraction, which is the amount of, uh, plasma that is filtered into the tubules at the glomerulus. The greater the fraction of plasma filtered through the glomerulus, and the more concentrated the protein becomes in the plasma that remains behind. So the higher the CF, the higher the amount of fluid that is filtered at the glomerulus, and the greater the concentration of the fluid left behind. Um. This increases the filtration fraction and the period tubular capillary reabsorption. Changes in the CF or the filtration coefficient can also change the Re absorption rate. The CF is a measure of the permeability and surface area of the capillaries, so increasing it raises reabsorption and decreasing lowers reabsorption. Uh working through this table, uh, which is table 28 two on page 357 and Guyton um can be a useful memory device. In general forces to increase paired tubular capillary reabsorption also increase reabsorption from the renal tubules. Conversely, hemodynamic changes that inhibit peri tubular capillary reabsorption also inhibit tubular reabsorption of water and solids. A decrease in the reabsorption in the tubular capillaries caused by either an increased in period tubular capillary hydrostatic pressure or a decrease in period tubular capillary colloid osmotic pressure reduces the uptake. Of fluid and solutes from the interstitium. This in turn decreases the uptake from the lumen. So this interstitial space here, if you increase these pressures or increase the hydrostatic pressure or decrease the colloid osmotic pressure, there's a normal uptake and you're pulling from the interstitium. Change these pressures. You can decrease this reabsorption from the interstitium. The decrease in reabsorption from this interstitium of course, uh, increases colloid osmotic pressure here or hydrostatic pressure and decreases the reabsorption from here. Want salutes and we'll further talk about that. Once salutes entered the interstitial channels by either active transport or passive diffusion. So this is here either by active transport or passive diffusion. Water is then drawn into the interstitial by osmosis. So uh water moves from here by osmosis. The solutes can be pulled into the period tubule capillaries here, as this arrow shows, or diffuse back in the air to the tubular lumen so they can go one of two ways. They either go this way or this way, obviously. Um. The size of this arrow does not have any relation to the strength of the attraction. Um. When paired to build capillary reabsorption is reduced. There is increased hydrostatic pressure and a tendency for solids to leak back into the tubular lumen. So if you decrease pair tubular reabsorption, increased pressure in the interstitium would happen. Increasing pressure in the interstitium obviously forces these solutes to head back out. When paired tube capillary absorption is increased the interstitial fluid. So if you did the opposite if you increase reabsorption this. Decreases. Decreases interstitial, uh, hydrostatic pressure, which increases reabsorption from here. Um. Changes in the pressure of the interstitium greatly affect the reabsorption from the tubular lumen. In pressure, natural eases and decreases. Small increases in arterial pressure can cause marked increases in urinary excretion of sodium and water. Between 75 and 160 arterial pressure. There is a small effect on renal blood flow and GFR. When the capillary hydrostatic pressure is increased, there is a decreased amount of reabsorption from the renal tubules. Third, due to increased are two a pressure angiotensin two formation is decreased, leading to decreased sodium reabsorption and decreased aldosterone secretion. And lastly, sodium transporter proteins are internalized. From the apical membranes of the renal tubule, so this was internalized by vessel and removed from the apical membrane. Uh uh, it's obviously not bringing in sodium from the tubule lumen. Uh, this is an example of a sodium chloride transporter in the, uh, distal tubules. Precise regulation of body fluid volumes and salute. Concentration requires the kidneys to excrete different solutes and water at variable rates. At times it must be able to do this while not affecting the retention or secretion of other solids. These are the most important hormones to provide that control. At the same time, stimulation of the sympathetic nervous system can also decrease sodium and water excretion. Now the Austrian is secreted by the zona glomerulus, the cells of the adrenal cortex, and increases the retention of sodium and water while secreting potassium and hydrogen ions. Now the Austrian stimulates a sodium potassium ATP pump on the basal lateral side of the cortical collecting tubule, while increasing sodium permeability on the apical side through the insertion of sodium channels. The most important stimuli for aldosterone release is increased extracellular potassium concentration and increased angiotensin two levels. Angiotensin two release is stimulated by low sodium or low blood volume or blood pressure. Angiotensin two and the resulting aldosterone causes renal sodium and water retention, restoring fluid and blood pressure. When there is an aldosterone deficiency, such as with Addison's disease, there's marked sodium loss and the accumulation of potassium, as opposed to Khan syndrome, which causes excessive aldosterone secretion and sodium retention and excessive secretion of potassium. Angiotensin two release is caused by low blood pressure or low extracellular fluid volume. It causes the retention of fluid and sodium mainly through these three effects. The constriction of arterials increases sodium and water reabsorption by reducing pair tubular capillary hydrostatic pressure, as well as decreasing renal blood flow, which raises the filtration fraction in the glomerulus. This increases the concentration of proteins and colloid osmotic pressure in the paired tubular capillaries. Angiotensin two stimulates sodium reabsorption in the proximal tubules, the loops of hennelly, the distal tubules, and collecting tubules by stimulating the sodium potassium pump on the basal lateral side of the tubular cells, just like our Doster shown on the previous slide. It also stimulates a sodium hydrogen exchanger on the luminal side in the proximal tubule. Angiotensin two stimulates sodium transport across both the apical and basal lateral surfaces of the epithelial cell membrane in most renal tubular segments. The most important renal action of ADH is to increase the water permeability of the distal tubule, collecting tubule and collecting duct epithelium. In the absence of 80 h, the permeability of the collecting ducts is low, causing the kidneys to excrete large amounts of diluted urine, otherwise known as diabetes insipidus. 80 h binds to specific V2 receptors that are G-protein coupled receptors that cause an increase cyclic adenosine monophosphate, or cyclic AMP and consequently activate protein kinase. These protein kinase is stimulate the placement of aquaporins two proteins on the luminal side of the cellular membrane by exocytosis. These water channels permit rapid diffusion of water through the cells. When the added concentration decreases, the aquaporins two molecules are removed and placed back in the cell cytoplasm. Eight year old natural peptide is released by cardiac atrial cells that are stretched by increased plasma volume and increased atrial blood pressure. ANP directly inhibit inhibits reabsorption of sodium and water by the renal tubules, especially in the collecting ducts, as well as the renal secretion and the subsequent formation of angiotensin two. By decreasing sodium and water absorption, urinary excretion is increased, which helps return the blood volume back to normal atrial naturally. Peptide levels are greatly increased in congestive heart failure when the atria are stretched due to decreased ventricular contraction. Parathyroid hormones. Principal action is to increase tubular reabsorption of calcium, especially in the distal and collecting tubules. It also inhibits phosphate reabsorption in the proximal tubule and increases magnesium absorption in the loop of. Sympathetic stimulation causes activation of alpha adrenergic receptors on the renal tubular epithelial cells. Stimulation also increases renin release and angiotensin two formation, which of course decreases the excretion of sodium. The renal clearance of a substance. Is the volume of plasma that is completely cleared of that substance by the kidneys per amount of time. It provides a useful way of quantifying excretory function of the kidneys. If there's one milligram of substance in each milliliter of plasma and one milligram is excreted into the urine each minute, then one milliliter a minute of the plasma is cleared. The formula is shown here and is calculated from the urine excretion rate, which is the urine concentration of that substance times the urinary flow rate divided by the plasma concentration. If a substance is freely filtered and is not reabsorbed or secreted. Then the rate at which it is excreted in the urine is equal to the filtration rate of the substance by the kidneys. GFR can be calculated using inulin since it is not reabsorbed or secreted. Therefore, all the inulin that is in the urine has been filtered. Ethical. Memoryless. In this illustration, the plasma concentration is 1mg/ml. The urine concentration is 125mg/ml, and the urine flow rate is one milliliter a minute. This means that 125mg a minute of insulin passes into the urine. Thus, 125ml of plasma flowing through the kidneys must be filtered to deliver that amount. Other substances have been used clinically to estimate GFR. And we will focus on the most common, which is creatinine. Creatinine is a byproduct of muscle metabolism and is cleared from the body almost entirely by glomerular filtration. Uh, since it is cleared almost entirely by glomerular filtration, it can be used to assess GFR. It's also not required to be given to the patient like insulin is um, it is secreted, uh, in small amounts by the tubules. So the amount excreted slightly exceeds the amount filtered. Uh, instead of measuring the creatine in urine, you can also measure the plasma concentration and estimate changes in GFR. Since a change in GFR will increase the plasma concentration under normal steady state conditions. Creatinine excretion, uh, equals the rate of creatinine production. Uh, the formula says that GFR is approximately equal to creating clearance, which is equal to the urine concentration of creatinine times urine flow rate, um, over the plasma concentration of creatinine. If a substance is completely cleared from the plasma, that clearance rate is equal to the total renal plasma flow. But since GFR is only about 20% of total plasma flow, if a substance is completely cleared from the plasma, it must be excreted by tubular secretion. The filtration fraction can also be calculated by dividing the GFR by the renal plasma flow. And lastly, the amount of tubular reabsorption or secretion can be calculated if the rates of Gomery filtration and renal excretion are known. For example, if the rates of excretion are less than what was filtered, then there must be some reabsorption. Conversely, if the rate of excretion exceeds the rate of filtration, then there must be some secretion in the tubes.