Countercurrent Exchange in the Vasa Recta Preserves Hyperosmolarity of the Renal Medulla

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Blood flow must be provided to the renal medulla to supply the metabolic needs of the cells in this part of the kidney. Without a special medullary blood flow system, the solutes pumped into the renal medulla by the countercurrent multiplier system would be rapidly dissipated.

There are two special features of the renal medullary blood flow that contribute to the preservation of the high solute concentrations:

1. The medullary blood flow is low, accounting for less than 5 per cent of the total renal blood flow. This sluggish blood flow is sufficient to supply the metabolic needs of the tissues but helps to minimize solute loss from the medullary interstitium.

2. The vasa recta serve as countercurrent exchangers, minimizing washout of solutes from the medullary interstitium.

The countercurrent exchange mechanism operates as follows (Figure 28-6): Blood enters and leaves the medulla by way of the vasa recta at the boundary of the cortex and renal medulla. The vasa recta, like other capillaries, are highly permeable to solutes in the blood, except for the plasma proteins. As blood descends into the medulla toward the papillae, it becomes progressively more concentrated, partly by solute entry from the interstitium and partly by loss of water into the interstitium. By the time the blood reaches the tips of the vasa recta, it has a concentration of about 1200 mOsm/L, the same as that of the medullary interstitium. As blood ascends back toward the cortex, it becomes progressively less concentrated as solutes diffuse back out into the medullary interstitium and as water moves into the vasa recta.

Thus, although there is a large amount of fluid and solute exchange across the vasa recta, there is little net dilution of the concentration of the interstitial fluid at each level of the renal medulla because of the U shape

State The Role Vasa Recta

Figure 28-6

Countercurrent exchange in the vasa recta. Plasma flowing down the descending limb of the vasa recta becomes more hyperos-motic because of diffusion of water out of the blood and diffusion of solutes from the renal interstitial fluid into the blood. In the ascending limb of the vasa recta, solutes diffuse back into the interstitial fluid and water diffuses back into the vasa recta. Large amounts of solutes would be lost from the renal medulla without the U shape of the vasa recta capillaries. (Numerical values are in milliosmoles per liter.)

Figure 28-6

Countercurrent exchange in the vasa recta. Plasma flowing down the descending limb of the vasa recta becomes more hyperos-motic because of diffusion of water out of the blood and diffusion of solutes from the renal interstitial fluid into the blood. In the ascending limb of the vasa recta, solutes diffuse back into the interstitial fluid and water diffuses back into the vasa recta. Large amounts of solutes would be lost from the renal medulla without the U shape of the vasa recta capillaries. (Numerical values are in milliosmoles per liter.)

of the vasa recta capillaries, which act as countercurrent exchangers. Thus, the vasa recta do not create the medullary hyperosmolarity, but they do prevent it from being dissipated.

The U-shaped structure of the vessels minimizes loss of solute from the interstitium but does not prevent the bulk flow of fluid and solutes into the blood through the usual colloid osmotic and hydrostatic pressures that favor reabsorption in these capillaries. Thus, under steady-state conditions, the vasa recta carry away only as much solute and water as is absorbed from the medullary tubules, and the high concentration of solutes established by the counter-current mechanism is maintained.

Increased Medullary Blood Flow Can Reduce Urine Concentrating Ability. Certain vasodilators can markedly increase renal medullary blood flow, thereby "washing out" some of the solutes from the renal medulla and reducing maximum urine concentrating ability. Large increases in arterial pressure can also increase the blood flow of the renal medulla to a greater extent than in other regions of the kidney and tend to wash out the hyperosmotic interstitium, thereby reducing urine concentrating ability. As discussed earlier, maximum concentrating ability of the kidney is determined not only by the level of ADH but also by the osmolarity of the renal medulla interstitial fluid. Even with maximal levels of ADH, urine concentrating ability will be reduced if medullary blood flow increases enough to reduce the hyperosmolarity in the renal medulla.

Summary of Urine Concentrating Mechanism and Changes in Osmolarity in Different Segments of the Tubules

The changes in osmolarity and volume of the tubular fluid as it passes through the different parts of the nephron are shown in Figure 28-7.

Proximal Tubule. About 65 per cent of the filtered electrolytes are reabsorbed in the proximal tubule. However, the tubular membranes are highly permeable to water, so that whenever solutes are reabsorbed, water also diffuses through the tubular membrane by osmosis. Therefore, the osmolarity of the fluid remains about the same as the glomerular filtrate, 300 mOsm/L.

Descending Loop of Henle. As fluid flows down the descending loop of Henle, water is absorbed into the medulla. The descending limb is highly permeable to water but much less permeable to sodium chloride and urea. Therefore, the osmolarity of the fluid flowing through the descending loop gradually increases until it is equal to that of the surrounding interstitial fluid, which is about 1200 mOsm/L when the blood concentration of ADH is high. When a dilute urine is being formed, owing to low ADH concentrations, the medullary interstitial osmolarity is less than 1200 mOsm/L; consequently, the descending loop tubular fluid osmo-larity also becomes less concentrated. This is due partly to the fact that less urea is absorbed into the medullary interstitium from the collecting ducts when ADH levels are low and the kidney is forming a large volume of dilute urine.

Thin Ascending Loop of Henle. The thin ascending limb is essentially impermeable to water but reabsorbs some sodium chloride. Because of the high concentration of sodium chloride in the tubular fluid, owing to water removal from the descending loop of Henle, there is some passive diffusion of sodium chloride from the thin ascending limb into the medullary interstitium. Thus, the tubular fluid becomes more dilute as the sodium chloride diffuses out of the tubule and water remains in the tubule. Some of the urea absorbed into the medullary interstitium from the collecting ducts also diffuses into the ascending limb, thereby returning the urea to the tubular system and helping to prevent its washout from the renal medulla. This urea recycling is an additional mechanism that contributes to the hyperosmotic renal medulla.

Thick Ascending Loop of Henle. The thick part of the ascending loop of Henle is also virtually impermeable to water, but large amounts of sodium, chloride, potassium, and other ions are actively transported from the tubule into the medullary interstitium. Therefore, fluid in the thick ascending limb of the loop of Henle becomes very dilute, falling to a concentration of about 100 mOsm/L.

Figure 28-7

Changes in osmolarity of the tubular fluid as it passes through the different tubular segments in the presence of high levels of antidiuretic hormone (ADH) and in the absence of ADH. (Numerical values indicate the approximate volumes in milliliters per minute or in osmolarities in mil-liosmoles per liter of fluid flowing along the different tubular segments.)

Early Distal Tubule. The early distal tubule has properties similar to those of the thick ascending loop of Henle, so that further dilution of the tubular fluid occurs as solutes are reabsorbed while water remains in the tubule.

Late Distal Tubule and Cortical Collecting Tubules. In the late distal tubule and cortical collecting tubules, the osmo-larity of the fluid depends on the level of ADH. With high levels of ADH, these tubules are highly permeable to water, and significant amounts of water are reabsorbed. Urea, however, is not very permeant in this part of the nephron, resulting in increased urea concentration as water is reabsorbed. This allows most of the urea delivered to the distal tubule and collecting tubule to pass into the inner medullary collecting ducts, from which it is eventually reabsorbed or excreted in the urine. In the absence of ADH, little water is reabsorbed in the late distal tubule and cortical collecting tubule; therefore, osmolarity decreases even further because of continued active reabsorption of ions from these segments.

Inner Medullary Collecting Ducts. The concentration of fluid in the inner medullary collecting ducts also depends on (1) ADH and (2) the osmolarity of the medullary interstitium established by the countercur-rent mechanism. In the presence of large amounts of ADH, these ducts are highly permeable to water, and water diffuses from the tubule into the interstitium until osmotic equilibrium is reached, with the tubular fluid having about the same concentration as the renal medullary interstitium (1200 to 1400 mOsm/L). Thus, a very concentrated but small volume of urine is produced when ADH levels are high. Because water reabsorption increases urea concentration in the tubular

Figure 28-7

Changes in osmolarity of the tubular fluid as it passes through the different tubular segments in the presence of high levels of antidiuretic hormone (ADH) and in the absence of ADH. (Numerical values indicate the approximate volumes in milliliters per minute or in osmolarities in mil-liosmoles per liter of fluid flowing along the different tubular segments.)

fluid, and because the inner medullary collecting ducts have specific urea transporters that greatly facilitate diffusion, much of the highly concentrated urea in the ducts diffuses out of the tubular lumen into the medullary interstitium. This absorption of the urea into the renal medulla contributes to the high osmo-larity of the medullary interstitium and the high concentrating ability of the kidney.

There are several important points to consider that may not be obvious from this discussion. First, although sodium chloride is one of the principal solutes that contributes to the hyperosmolarity of the medullary interstitium, the kidney can, when needed, excrete a highly concentrated urine that contains little sodium chloride. The hyperosmolarity of the urine in these circumstances is due to high concentrations of other solutes, especially of waste products such as urea and creatinine. One condition in which this occurs is dehydration accompanied by low sodium intake. As discussed in Chapter 29, low sodium intake stimulates formation of the hormones angiotensin II and aldos-terone, which together cause avid sodium reabsorption from the tubules while leaving the urea and other solutes to maintain the highly concentrated urine.

Second, large quantities of dilute urine can be excreted without increasing the excretion of sodium. This is accomplished by decreasing ADH secretion, which reduces water reabsorption in the more distal tubular segments without significantly altering sodium reabsorption.

And finally, we should keep in mind that there is an obligatory urine volume, which is dictated by the maximum concentrating ability of the kidney and the amount of solute that must be excreted. Therefore, if large amounts of solute must be excreted, they must be accompanied by the minimal amount of water necessary to excrete them. For example, if 1200 mil-liosmoles of solute must be excreted each day, this requires at least 1 liter of urine if maximal urine concentrating ability is 1200 mOsm/L.

Quantifying Renal Urine Concentration and Dilution: "Free Water" and Osmolar Clearances

The process of concentrating or diluting the urine requires the kidneys to excrete water and solutes somewhat independently. When the urine is dilute, water is excreted in excess of solutes. Conversely, when the urine is concentrated, solutes are excreted in excess of water.

The total clearance of solutes from the blood can be expressed as the osmolar clearance (Cosm); this is the volume of plasma cleared of solutes each minute, in the same way that clearance of a single substance is calculated:


Uosm X V

Pos where Uosm is the urine osmolarity, V is the urine flow rate, and Posm is the plasma osmolarity. For example, if plasma osmolarity is 300 mOsm/L, urine osmolarity is 600 mOsm/L, and urine flow rate is 1 ml/min (0.001 L/ min), the rate of osmolar excretion is 0.6 mOsm/min (600 mOsm/L X 0.001 L/min) and osmolar clearance is 0.6 mOsm/min divided by 300 mOsm/L, or 0.002 L/min (2.0 ml/min). This means that 2 milliliters of plasma are being cleared of solute each minute.

Relative Rates at Which Solutes and Water Are Excreted Can Be Assessed Using the Concept of "Free-Water Clearance." Free-water clearance (Ch2c>) is calculated as the difference between water excretion (urine flow rate) and osmolar clearance:

Thus, the rate of free-water clearance represents the rate at which solute-free water is excreted by the kidneys. When free-water clearance is positive, excess water is being excreted by the kidneys; when free-water clearance is negative, excess solutes are being removed from the blood by the kidneys and water is being conserved.

Using the example discussed earlier, if urine flow rate is 1 ml/min and osmolar clearance is 2 ml/min, free-water clearance would be -1 ml/min. This means that instead of water being cleared from the kidneys in excess of solutes, the kidneys are actually returning water back to the systemic circulation, as occurs during water deficits. Thus, whenever urine osmolarity is greater than plasma osmolarity, free-water clearance will be negative, indicating water conservation.

When the kidneys are forming a dilute urine (that is, urine osmolarity is less than plasma osmolarity), free-water clearance will be a positive value, denoting that water is being removed from the plasma by the kidneys in excess of solutes. Thus, water free of solutes, called "free water," is being lost from the body and the plasma is being concentrated when free-water clearance is positive.

Disorders of Urinary Concentrating Ability

An impairment in the ability of the kidneys to concentrate or dilute the urine appropriately can occur with one or more of the following abnormalities:

1. Inappropriate secretion of ADH. Either too much or too little ADH secretion results in abnormal fluid handling by the kidneys.

2. Impairment of the countercurrent mechanism. A hyperosmotic medullary interstitium is required for maximal urine concentrating ability. No matter how much ADH is present, maximal urine concentration is limited by the degree of hyperosmolarity of the medullary interstitium.

3. Inability of the distal tubule, collecting tubule, and collecting ducts to respond to ADH.

Failure to Produce ADH: "Central" Diabetes Insipidus. An inability to produce or release ADH from the posterior pituitary can be caused by head injuries or infections, or it can be congenital. Because the distal tubular segments cannot reabsorb water in the absence of ADH, this condition, called "central" diabetes insipidus, results in the formation of a large volume of dilute urine, with urine volumes that can exceed 15 L/day. The thirst mechanisms, discussed later in this chapter, are activated when excessive water is lost from the body; therefore, as long as the person drinks enough water, large decreases in body fluid water do not occur. The primary abnormality observed clinically in people with this condition is the large volume of dilute urine. However, if water intake is restricted, as can occur in a hospital setting when fluid intake is restricted or the patient is unconscious (for example, because of a head injury), severe dehydration can rapidly occur.

The treatment for central diabetes insipidus is administration of a synthetic analog of ADH, desmopressin, which acts selectively on V2 receptors to increase water permeability in the late distal and collecting tubules. Desmopressin can be given by injection, as a nasal spray, or orally, and rapidly restores urine output toward normal.

Inability of the Kidneys to Respond to ADH: "Nephrogenic" Diabetes Insipidus. There are circumstances in which normal or elevated levels of ADH are present but the renal tubular segments cannot respond appropriately. This condition is referred to as "nephrogenic" diabetes insipidus because the abnormality resides in the kidneys. This abnormality can be due to either failure of the countercurrent mechanism to form a hyperosmotic renal medullary interstitium or failure of the distal and collecting tubules and collecting ducts to respond to ADH. In either case, large volumes of dilute urine are formed, which tends to cause dehydration unless fluid intake is increased by the same amount as urine volume is increased.

Many types of renal diseases can impair the concentrating mechanism, especially those that damage the renal medulla. Also, impairment of the function of the loop of Henle, as occurs with diuretics that inhibit electrolyte reabsorption by this segment, can compromise urine concentrating ability. And certain drugs, such as lithium (used to treat manic-depressive disorders) and tetracyclines (used as antibiotics), can impair the ability of the distal nephron segments to respond to ADH.

Nephrogenic diabetes insipidus can be distinguished from central diabetes insipidus by administration of desmopressin, the synthetic analog of ADH. Lack of a prompt decrease in urine volume and an increase in urine osmolarity within 2 hours after injection of desmopressin is strongly suggestive of nephrogenic diabetes insipidus. The treatment for nephrogenic diabetes insipidus is to correct, if possible, the underlying renal disorder. The hypernatremia can also be attenuated by a low-sodium diet and administration of a diuretic that enhances renal sodium excretion, such as a thiazide diuretic.

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    How countercurrent prevents washout of solutes?
    4 years ago
  • becky
    How the u shape vasa recta make the medulla hyperosmolar?
    4 years ago
  • anita balzer
    How vasa recta preserves hyperosmolarity?
    4 years ago
  • emma
    Why u shaped structure of vasa recta?
    4 years ago
  • Maik
    How counter current flow prevents washouts?
    4 years ago
  • jenni
    How does a counter current prevent wash out?
    4 years ago
  • Gundabald Lothran
    How does increased medullary blood flow reduce urine concentrating ability?
    4 years ago
    What will happen of blood flow inn vasa recta increases or decreases and why?
    4 years ago
  • steven
    What is the aim of maintained medullary hyperosmolarity?
    4 years ago
  • Pauli
    How increasing medullary blood flow decreases medullary interstitium osmolarity?
    4 years ago
  • Claudia
    How is interstitial osmolality maintained when vasa recta take all solutes out of ascending limb?
    4 years ago
  • Ilta
    Why interstitial fluid becomes more concentrated in renal medulla?
    4 years ago
    How vasa recta contributes to formation of concentrated urine?
    4 years ago
  • kerstin
    What is the role of the vasa recta in controlling the concentration of urine?
    4 years ago
  • Justiina
    How does vasa recta maintain a countercurrent exchange?
    4 years ago
  • Margarette
    Why blood pressure is low in vasa recta?
    4 years ago
  • demi
    How osmolarity of medula interstium is maintain by vasa recta?
    4 years ago
    Why there is same osmolarity of 1200 in interstitial fluid and blood?
    4 years ago
  • Meriadoc
    Why hyperosmolarity of renal medullary is needed?
    4 years ago
  • marta
    How vasa recta help to produce concentrated urine?
    3 years ago
  • luam
    What is the function of the vasa recta in nephrone?
    3 years ago
  • Viola Colombo
    Why is the vasa recta called the countercurrent exchanger?
    3 years ago
    What prevents washout of solutes from kidney?
    3 years ago
  • Wayne
    What is the function of vasa recta in humans?
    3 years ago
    Is hyperosmolar medullary interstitium also related to ADH?
    3 years ago
  • yonas
    What will happen if blood flow in thw vasa recta is increased?
    3 years ago
  • william
    How hyperosmolarity in medullary interstitium?
    3 years ago
  • Alice
    What will happen to urine if blood flow in vasa recta is decreased?
    3 years ago
  • viola
    Why does the NaCl does not into the ascending loop of vasa recta?
    3 years ago
  • Jamie-leigh
    How osmolarity is maintained in renal interistium?
    3 years ago
  • Sophie
    What happens in counter current exchanger?
    3 years ago
  • gilly
    What is the counter current exchanger in the vasarecta?
    3 years ago
  • jan
    How vasa recta maintain hyperosmolarity of the medull?
    3 years ago
  • jago smallburrow
    How sluggish blood flow maintains hyperosmotic medullary interstitium in kidneys?
    3 years ago
  • Sherry
    How does countercurrent flow prevent washout?
    3 years ago
  • edilio toscani
    Why solute loss in ascending vasa recta?
    3 years ago
  • teresio
    How the vasa recta capillariesWork as a counter current exchanger?
    2 years ago
  • alfrida
    What is countercurrent exchange occurs in the vasa recta?
    2 years ago
  • jan v
    Why is hyperosmolarity decrease in ascending vasa recta?
    11 months ago
  • Connor
    How does the countercurrent exchanger maintain medulla?
    3 months ago
    What is the current exchange mechanism of the loop of henle?
    2 months ago
  • Celso
    What type of transport is causing this flow of water and ions in the vasa recta?
    2 months ago
  • Aune
    How does countercurrent exchange facilitate excretion?
    1 month ago
  • fesahaye
    Where does counter current flow in human being occur?
    1 month ago
    How does countercurrent exchange mechanism in the vasa recta operate to minimize washout of solutes?
    4 days ago

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