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Urophysiology 5

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control of ECF osmolarity & Regulation of electrolytes

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Urophysiology 5

  1. 1. CONTROL OF EXTRACELLULAR FLUID OSMOLARITY AND SODIUM CONCENTRATION • Regulation of extracellular fluid osmolarity and sodium concentration are closely linked because sodium is the most abundant ion in the extracellular compartment. • Plasma sodium concentration is normally regulated within close limits of 140 to 145 mEq/L. • Sodium ions and associated anions (primarily bicarbonate and chloride) represent about 94 percent of the extracellular osmoles, with glucose and urea contributing about 3 to 5 percent 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.
  2. 2. 1- OSMORECEPTOR-ADH FEEDBACK SYSTEM
  3. 3. ADH synthesis in supraoptic and paraventricular nuclei of the hypothalamus and ADH release from the posterior pituitary. • STIMULATION OF ADH RELEASE BY: 1. Increased osmolarity. 2. Decreased arterial pressure. 3. Decreased blood volume
  4. 4. 2- IMPORTANCE OF THIRST IN CONTROLLING EXTRACELLULAR FLUID OSMOLARITY AND SODIUM CONCENTRATION: • The kidneys minimize fluid loss during water deficits through the osmoreceptor-ADH feedback system. • Adequate fluid intake, however, is necessary to counterbalance whatever fluid loss does occur through sweating and breathing and through the gastrointestinal tract. • Many of the same factors that stimulate ADH secretion also increase thirst, which is defined as the conscious desire for water.
  5. 5. • STIMULI FOR THIRST: 1. Increased extracellular fluid osmolarity, which causes intracellular dehydration in the thirst centers, thereby stimulating the sensation of thirst. 2. Decreases in extracellular fluid volume and arterial pressure also stimulate thirst. 3. A third important stimulus for thirst is angiotensin II. 4. Dryness of the mouth and mucous membranes of the esophagus can elicit the sensation of thirst. 5. Gastrointestinal and pharyngeal stimuli influence thirst. After a person drinks water, 30 to 60 minutes may be required for the water to be reabsorbed and distributed throughout the body. If the thirst sensation were not temporarily relieved after drinking water, the person would continue to drink more and more, eventually leading to overhydration and excess dilution of the body fluids.
  6. 6. • Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium. • Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume.
  7. 7. 1- Regulation of extracellular fluid potassium concentration and potassium excretion: • Extracellular fluid potassium concentration normally is regulated at about 4.2 mEq/L. • Maintenance of balance between intake and output of potassium depends primarily on excretion by the kidneys.
  8. 8. • The most important factors that stimulate potassium secretion by the principal cells include: (1) Increased extracellular fluid potassium concentration. (2) Increased aldosterone. (3) Increased tubular flow rate. • One factor that decreases potassium secretion is increased hydrogen ion concentration (acidosis). Renal potassium excretion is determined by the sum of three processes: (1) the rate of potassium filtration (glomerular filtration rate [GFR] multiplied by the plasma potassium concentration), (2) the rate of potassium reabsorption by the tubules, and (3) the rate of potassium secretion by the tubules.
  9. 9. Increased dietary potassium intake and increased extracellular fluid potassium concentration stimulate potassium secretion by four mechanisms: 1. sodium-potassium ATPase pump, causing potassium to diffuse across the luminal membrane into the tubule. 2. increases the potassium gradient from the renal interstitial fluid to the interior of the epithelial cell, which reduces backleakage of potassium ions from inside the cells. 3. synthesis of potassium channels. 4. stimulates aldosterone secretion by the adrenal cortex.
  10. 10. 1 2 34
  11. 11. • Hypocalcemia increase the excitability of nerve and muscle cells result in hypocalcemic tetany. • Hypercalcemia depresses neuromuscular excitability and can lead to cardiac arrhythmias. A. 50 percent in the plasma = ionized form. B. 40 percent = bound to the plasma proteins. C. 10 percent = complexed in the non-ionized form with anions such as phosphate and citrate. • The usual rate of dietary calcium intake is about 1000 mg/day, with about 900 mg/day of calcium excreted in the feces. 2- Control of renal calcium excretion and extracellular calcium ion concentration:
  12. 12. A. 99 % stored in the bone. B. 0.1 % in the extracellular fluid. C. 1.0 % in the intracellular fluid and cell organelles. • One of the most important regulators of bone uptake and release of calcium is PTH. • PTH regulates plasma calcium concentration through three main effects: (1) by stimulating bone resorption. (2) by stimulating activation of vitamin D, which then increases intestinal reabsorption of calcium. (3) by directly increasing renal tubular calcium reabsorption.
  13. 13. • Renal calcium excretion = Calcium filtered – Calcium reabsorbed. • Normally, about 99 % of calcium is reabsorbed, only 1% of calcium is excreted. • Percentage of calcium reasbsorption: 1. 65% reabsorbed in the proximal tubule. 2. 25 to 30% is reabsorbed in the loop of Henle. 3. 4 to 9% is reabsorbed in the distal and collecting tubules.
  14. 14. • When less than 0.1 mmol/min amount of phosphate is present in the glomerular filtrate, essentially all the filtered phosphate is reabsorbed. • When more than 0.1 mmol/min amount is present, the excess is excreted. • Most people ingest large quantities of phosphate in milk products and meat. • 75 to 80% is reabsorbed by proximal tube. • 10 % is reabsorbed by distal tubule • 1% are reabsorbed in the loop of Henle, collecting tubules, and collecting ducts. • 10% of the filtered phosphate is excreted in the urine. 3- regulation of renal phosphate excretion
  15. 15. • PTH can play a significant role in regulating phosphate concentration through two effects: (1) PTH promotes bone resorption, thereby dumping large amounts of phosphate ions into the extracellular fluid from the bone salts. (2) PTH decreases the transport maximum for phosphate by the renal tubules, so a greater proportion of the tubular phosphate is lost in the urine. • Whenever plasma PTH is increased, tubular phosphate reabsorption is decreased and more phosphate is excreted. • Phosphate enters the cell from the lumen by a sodium-phosphate co-transporter and exits the cell across the basolateral membrane by a process that is not well understood.
  16. 16. • More than one half of the body’s magnesium is stored in the bones. • Although the total plasma magnesium concentration is about 1.8 mEq/L, more than one half of this is bound to plasma proteins. • Therefore, the free ionized concentration of magnesium is only about 0.8 mEq/L. • The normal daily intake of magnesium is about 250 to 300 mg/day. • Magnesium is involved in many biochemical processes in the body, including activation of many enzymes, its concentration must be closely regulated. • The following disturbances lead to increased magnesium excretion: (1) Increased extracellular fluid magnesium concentration. (2) Extracellular volume expansion. (3) increased extracellular fluid calcium concentration. 4- Control of renal magnesium excretion and extracellular magnesium ion concentration.
  17. 17. • Extracellular fluid volume is determined mainly by the balance between intake and output of water and salt. • Pressure diuresis: refers to the effect of increased blood pressure to raise urinary volume excretion. • Pressure natriuresis: refers to the rise in sodium excretion that occurs with elevated blood pressure.
  18. 18. The Basic Renal–body Fluid Feedback Mechanism:
  19. 19. DISTRIBUTION OF EXTRACELLULAR FLUID BETWEEN THE INTERSTITIAL SPACES AND VASCULAR SYSTEM: • Ingested fluid initially goes into the blood, but it rapidly becomes distributed between the interstitial spaces and the plasma. • Accumulation of fluid in the interstitial spaces by these factors: (1) increased capillary hydrostatic pressure. (2) decreased plasma colloid osmotic pressure. (3) increased permeability of the capillaries. (4) obstruction of lymphatic vessels.
  20. 20. Role Of Hormones In Regulating Renal Excretion: A) ROLE OF ANG II IN CONTROLLING RENAL EXCRETION: • Increased levels of Ang II cause sodium and water retention & also increase in arterial blood pressure. • Decreased levels of Ang II cause sodium and water excretion & also reduction in arterial blood pressure. B) ROLE OF ALDOSTERONE IN CONTROLLING RENAL EXCRETION: • Increased levels of Aldosterone cause sodium and water reabsorption + secretion of potassium. • Decreased levels of Aldosterone cause sodium and water excretion + reabsorption of potassium.
  21. 21. C) ROLE OF ADH IN CONTROLLING RENAL WATER EXCRETION: • Increased level of ADH causes reabsorption of water and excretion large amount of Sodium and increase arterial pressure. • Decreased level of ADH causes decreased reabsorption of water and excretion small amount of Sodium and slightly decreased arterial pressure. D) ROLE OF ATRIAL NATRIURETIC PEPTIDE IN CONTROLLING RENAL EXCRETION: • Increased level of ANP causes increased excretion of salt and water. • Decreased level of ANP causes decreased excretion of salt and water.
  22. 22. • Conditions That Cause Large Increases In Blood Volume And Extracellular Fluid Volume: 1. Heart diseases. 2. Increased capacity of circulation (pregnancy & varicose vein in leg). • Conditions That Cause Large Increases In Extracellular Fluid Volume But With Normal Blood Volume: 1. Nephrotic syndrome—loss of plasma proteins in urine and sodium retention by the kidneys 2. Liver cirrhosis—decreased synthesis of plasma proteins by the liver and sodium retention by the kidneys.

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