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Urine Concentration and Dilution; Regulation of Extracellular Fluid Osmolarity and Sodium Concentration The body water is controlled by:
ā¢ Fluid intake, which is regulated by factors that determine thirst.
ā¢ Renal excretion of water 0 3 3 60 3 3 6controlled by multiple factors that influence glomerular filtration and tubular reabsorption.
The Kidneys Excrete Excess Water By Forming Dilute Urine *When there is excess water in the body
- When body fluid osmolarity is reduced The kidney can excrete urine with an osmolarity as low as 50 mOsm/L, a concentration that is only about one sixth the osmolarity of normal extracellular fluid. Conversely,
ā¢ when there is a deficit of water
ā¢ when extracellular fluid osmolarity is high, the kidney can excrete urine with a concentration of 1200 to 1400 mOsm/L
Renal Mechanisms for Excreting Dilute Urine When there is a large excess of water in the body, the kidney can excrete as much as 20 L/day of dilute urine. The kidney performs this by continuing to reabsorb solutes while failing to reabsorb large amounts of water in the distal parts of the nephron, (late distal tubule and the collecting ducts).
ā¢ Formation of dilute urine when antidiuretic hormone (ADH) levels are very low in the ascending loop of Henle.
The failure to reabsorb water and continued reabsorption of solutes lead to a large volume of dilute urine.
Tubular Fluid in Distal and Collecting Tubules In the absence of ADH, distal and collecting tubules is also impermeable to water, and the additional reabsorption of solutes causes the tubular fluid to become more dilute, āā its osmolarity to as low as 50 mOsm/L. *The failure to reabsorb water and the continued reabsorption of solutes will lead to a large volume of dilute urine.
Summary:
ā¢ In healthy kidneys, fluid leaving the ascending loop of Henle and early distal tubule is always dilute, regardless of the level
of ADH.
ā¢ In the absence of ADH, the urine is further diluted in the late distal tubule and collecting ducts and a large volume of dilute
urine is excreted.
Kidneys Conserve Water by Excreting Concentrated Urine The ability of the kidney to form concentrated urine is important for survival of humans living on land. When there is a water deficit in the body, the kidney forms concentrated urine by continuing to excrete solutes while increasing water reabsorption and decreasing the volume of urine formed. The human kidney can produce a maximal urine concentration of 1200 to 1400 mOsm/L, four to five times the osmolarity of plasma.
Formation of a concentrated urine-- Antidiuresis
ā¢ Continue electrolyte reabsorption
ā¢ Increase water
ā¢ reabsorption
Maximal urine concentration = 1200 to 1400mOsm/L (Specific gravity ~ 1.030) Formation of a dilute urine-- Diuresis
ā¢ Continue electrolyte reabsorption
ā¢ Decrease water reabsorption
Minimal urine concentration = 50 - 70mOsm/L (Specific gravity ~ 1.003)
Obligatory Urine Volume The minimal volume of urine that must be excreted, called the obligatory urine volume. A normal 70-kilogram human must excrete about 600 milliosmoles of solute each day. If maximal urine concentrating ability is1200mOsm/L, 600 mOsm day 0 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 6 = 0.5 L day (obligatory urine volume) 1200 mOsm L
ā¢ What happen if subject drinks sea water?
Sodium chloride concentration in the oceans averages about 3.0 to 3.5%, with an osmolarity between about 1000 -1200 mOsm/L. Drinking 1 liter of seawater with a concentration of 1200 mOsm/L would provide a total sodium chloride intake of 1200 mOsm. If maximal urine concentrating ability is 1200 mOsm/L, the amount of urine volume needed to excrete 1200 mOsm would be 1200 mOsm 0 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 60 3 3 6 = 1.0 L 1200 mOsm/L
ā¢ Why does drinking seawater cause dehydration?
The kidney must also excrete other solutes (urea) which contribute about 600mOsm/L when the urine is maximally concentrated. Therefore, the maximum concentration of sodium chloride that can be excreted by the kidneys is about 600mOsm/L. Mean for every liter of seawater drunk, 2 liters of urine volume would be required to rid the body of 1200 milliosmoles of sodium chloride ingested in addition to other solutes such as urea.
Urine Specific Gravity
ā¢ Urine Solute Concentration
ā¢ The measure of weight of solutes in a given volume of urine and is therefore determined only by the number and size of the
solute molecules. Normal range: 1.002- 1. Rising by 0.001 for every 35- 45mOsmol/L increase in urine concentration. Osmolarity
ā¢ Determined only by the number of solute molecules in a given volume.
Requirements for Excreting Concentrated Urine
1. A high level of ADH
This increases the permeability of the distal tubules and collecting ducts to water.
2. A high osmolarity of the renal medullary interstitial fluid
This provides the osmotic gradient necessary for water reabsorption to occur in the presence of high levels of ADH. Antidiuretic Hormone (ADH): Vasopressin When osmolarity of the body fluids increases above normal (that is, the solutes in the body fluids become concentrated), the posterior pituitary gland secretes more ADH, which increases the permeability of the distal tubules and collecting ducts to water This
The countercurrent exchange mechanism in the Vasa Recta Preserves Hyperosmolarity of the Renal Medulla 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.
Less than 5% of 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 medullary interstitium.
2. The vasa recta serve as countercurrent exchangers
This minimizes the washout of solutes from the medullary interstitium.
*Plasma flowing down the descending limb of the vasa recta becomes more hyperosmotic 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.
SUMMARY:
ā¢ Proximal Tubule: 65 % of the filtered
Electrolytes are reabsorbed in the proximal tubule. (The osmolarity of the fluid the same as the glomerular filtrate, 300 mOsm/L)
ā¢ Descending Loop of Henle:
The descending limb is highly permeable to water but much less permeable to sodium chloride and urea The osmolarity is about 1200 mOsm/L.
ā¢ Thin Ascending Loop of Henle:
The thin ascending limb is impermeable to water but reabsorbs some sodium chloride. 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. The longer the loop, the more concentrated the filtrate and the medullary IF become. Importance: The collecting tubule runs through the hyperosmotic medulla more ability to reabsorb H 2 O.
ā¢ 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.
ā¢ Early Distal Tubule
The early distal tubule has properties similar to thick ascending loop of Henle, further dilution of the tubular fluid occurs (Solutes are reabsorbed while water remains in the tubule).
ā¢ Late Distal Tubule and Cortical Collecting Tubules
The osmolarity of the fluid depends on the level of ADH. (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).
ā¢ Inner medullary collecting ducts
Osmolarity depends on (1) ADH (when ADH levels are high small volume of urine produced). (2) The osmolarity of the medullary interstitium established by the countercurrent mechanism. (the renal medullary interstitium (1200 -1400 mOsm/L).
Disorders of Urinary Concentrating Ability
1. Inappropriate secretion of ADH. (Too much or too little ADH)
2. Impairment of the countercurrent mechanism.
A hyperosmotic medullary interstitium is required for maximal urine concentrating ability (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.
Inability of the Kidneys to Respond to ADH: Nephrogenic Diabetes Insipidus. Failure of countercurrent mechanism to form hyperosmotic renal medullary interstitium or failure of the distal and collecting tubules and collecting ducts to respond to ADH. Many types of renal diseases can impair the concentrating mechanism,
ā² Damage of the renal medulla
ā² 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.
ā² Certain drugs, such as lithium (used to treat manic-depressive disorders) and tetracyclines impair the ability of the distal
nephron segments to respond to ADH.
Control of Extracellular Fluid Osmolarity and Sodium Concentration
ā¢ Normal Plasma Sodium Concentration = 140 - 145 mEq/L, average about 142mEq/L.
ā¢ Osmolarity averages about 300mOsm/L
ā² Sodium and its associated anions account for about 94 % of the solute in the extracellular compartment.
ā² Glucose and urea contributing about 3 - 5 % of the total osmoles.
Two primary systems are especially involved in regulating the concentration of sodium and osmolarity of extracellular fluid:
(1) The osmoreceptor-ADH system
(2) The thirst mechanism
Fluid intake is regulated by the thirst mechanism, which, together with the osmoreceptorĀ¬ADH mechanism, mainĀ¬ tains precise control of extracellular fluid osmolarity and sodium concentration
Central Nervous System for Thirst The same area along the anteroventral wall of the third ventricle that promotes 384 ADH release also stimulates thirst. When stimulated electrically, causes immediate drinking that continues as long as the stimulation lasts. All these areas together are called the thirst center. The neurons of the thirst center respond to injections of hypertonic salt solutions by stimulating drinking behavior. These cells almost certainly function as osmoreceptors to activate the thirst mechanism, in the same way that the osmoreceptors stimulate ADH release. Increased osmolarity of the cerebrospinal fluid in the third ventricle has essentially the same effect to promote drinking. It is likely that the organum vasculosum of the lamina terminalis, which lies immediately beneath the ventricular surface at the inferior end of the AV3V region, is intimately involved in mediating this response.
Threshold for Drinking When the sodium concentration increases only about 2 mEq/L above normal, the thirst mechanism is activated, causing a desire to drink water.
Thirst Mechanism in Controlling ECF Osmolarity and Sodium Concentration When either the ADH or the thirst mechanism fails, the other ordinarily can still control extracellular osmolarity and sodium concentration with reasonable effectiveness, as long as there is enough fluid intakes to balance the daily obligatory urine volume and water losses caused by respiration, sweating, or gastrointestinal losses. However, if both the ADH and thirst mechanisms fail simultaneously, plasma sodium concentration and osmolarity are poorly controlled; thus, when sodium intake is increased after blocking the total ADH- thirst system, large changes in plasma sodium concentration occur. In the absence of the ADH thirst mechanisms, no other feedback mechanism is capable of adequately regulating plasma sodium concentration and osmolarity.
Role of Angiotensin II and Aldosterone in Controlling Extracellular Fluid Osmolarity and Sodium Concentration Both angiotensin II and aldosterone play an important role in regulating sodium reabsorption by the renal tubules. When sodium intake is low, increased levels of these hormones stimulate sodium reabsorption by the kidneys and, therefore, prevent large sodium losses, even though sodium intake may be reduced to as low as 10 per cent of normal. Conversely, with high sodium intake, decreased formation of these hormones permits the kidneys to excrete large amounts of sodium.
Salt-Appetite Mechanism for Controlling ECF Sidium Concentration and Volume Two primary stimuli that are believed to increase salt appetite are
1. Decreased extracellular fluid sodium concentration
2. Decreased blood volume or blood pressure, associated with circulatory insufficiency.
Maintenance of normal extracellular fluid volume and sodium concentration requires a balance between sodium excretion and sodium intake. In modern civilizations, sodium intake is almost always greater than necessary for homeostasis. In fact, the average sodium intake for individuals in industrialized cultures eating processed foods usually ranges between 100 and 200 mEq/day, even though
humans can survive and function normally on 10 to 20 mEq/day. Thus, most people eat far more sodium than is necessary for homeostasis, and there is evidence that our usual high sodium intake may contribute to cardiovascular disorders such as hypertension.
Explain the effect of 1- primary aldosteronism 2-adrenalectomy or in patients with Addisonās disease (severely impaired secretion or total lack of aldosterone).
