Block: URIN 313 Physiology of THE URINARY SYSTEM Lecture 8

1. Block: URIN 313Physiology of THE URINARY SYSTEM Lecture 8 • Dr. AmelEassawi • Dr. ShaikhMujeeb Ahmed

2. DILUTING AND CONCENTRATING URINE MECHANISM

3. OBJECTIVES • The student should be able to: • Describe the factors that determine the ability of loop of Henle to create osmotic medullary gradient. • Identify countercurrent multiplier and countercurrent exchange systems in concentrating and diluting urine. • Explain changes in osmolarity of tubular fluid in the various segments of the loop of Henle when concentrated urine is being produced. • Describe the role of ADH on the ability of the kidney to produce either a dilute or a concentrated urine. • Discuss the micturition reflex.

4. Urine Excretion • Depending on the body’s state of hydration, the kidneys secrete urine of varying concentrations. • Too much water in the ECF establishes a hypotonic ECF. • A water deficit establishes a hypertonic ECF. • This function is determined by the amount of water reabsorption in the renal tubules.

5. Urine Concentration AND Dilution • Water reabsorption is obligatory in the proximal (65%) tublues and Loop of Henle(15%). • The final adjustment of the urine volume and osmolarity depends on the extent of facultative water reabsorption in the Collecting Ducts, which is depends on:- • The blood level of antidiuretic hormone (ADH). • The medullaryinterstitium (MI) hypertonicity (Medullary concentration gradient).

6. Urine Concentration Requirements for forming a concentrated urine are: • High level of ADH (increase permeability) • High osmolarity of the renal medullary interstitial fluid (osmotic gradients. • Driving force for water reabsorption throughout the entire length of tubules is the osmotic gradient between tubular lumen and surrounding interstitial fluid.

7. A large, vertical osmotic gradient is established in the interstitial fluid of the medulla (from 100 to 1200 mosm/liter) This osmotic gradient exists between the tubular lumen and the surrounding interstitial fluid.

8. Medullary Countercurrent system • JuxtaMedullaryNephrons • long loop of henleestabilishes a vertical osmotic gradient (Countercurrent multiplier) , their vassa recta preserve this gradient while providing blood to renal medulla ( Countercurrent exchanger). • collecting ducts of all nephrones use the gradient in conjunction with the hormone vassopressin, to produce urine of varying concentration (osmotic equilibrating device) . • Collectively this entire functional organization is known as medullary countercurrent system

9. Countercurrent Multiplication • Comparing the descending and ascending limbs of the loop of Henle. • The descending ling is highly permeable to water but does not extrude sodium for reabsorption. • The ascending limb actively transports NaClout of the tubular lumen into the surrounding interstitial fluid. It is impermeable to water. Therefore, water does not follow the salt by osmosis. • There is a countercurrent flow produced by the close proximity of the two limbs.

10. Countercurrent Multiplication

11. Countercurrent Multiplication

12. Countercurrent Multiplication

13. Countercurrent Multiplication

14. Countercurrent Multiplication

15. Countercurrent Multiplication

16. Countercurrent Multiplication

17. BENEFITS OF COUNTERCURRENT MULTIPLICATION It establishes a vertical osmotic gradient in the medullary interstitial fluid. This gradient, in turn, is used by the collecting ducts to concentrate the tubular fluid so that a urine more concentrated than normal body fluids can be excreted. Second, the fact that the fluid is hypotonic as it enters the distal parts of the tubule enables the kidneys to excrete a urine more dilute than normal body fluids.

18. Role of Vasopressin • Vasopressin-controlled, variable water reabsorption occurs in the final tubular segments. • 65 % of water reabsorption is obligatory in the proximal tubule. • In the distal tubule and collecting duct is variable, based on the secretion of ADH. • The secretion of vasopressin increases the permeability of the tubule cells to water. An osmotic gradient exists outside the tubules for the transport of water by osmosis. • Vasopressin works on tubule cells through a cyclic AMP mechanism. • During a water deficit, the secretion of vasopressin increases. This increases water reabsorption. During an excess of water, the secretion of vasopressin decreases. Less water is reabsorbed. More is eliminated.

19. Mechanism of action of Vasopressin

20. Urea Recirculation • Urea is passively reabsorbed in proximal tubule. • In the presence of ADH, water is reabsorbed in distal and collecting tubules, concentrating urea in these parts of the nephron. • The inner medullary collecting tubule is highly permeable to urea, which diffuses into the medullaryinterstitium. • ADH increases urea permeability of medullary collecting tubule.

21. Recirculation of Urea Absorbed from MedullaryCollecting Duct into Interstitial Fluid

22. Regulation of H2O reabsorption in response to H2O deficit

23. Regulation of H2O reabsorption in response to H2O Excess

24. Countercurrent exchange within the vasa recta conserves the medullary vertical osmotic gradient.

25. The Vasa Recta Preserve Hyperosmolarity of Renal Medulla • The vasa recta serve as countercurrent exchangers • Vasa recta blood flow is low (only 1-2 % of total renal blood flow)

26. Renal Failure • Causes of Renal Failure • - Infectious organisms • - Toxic agents • - Inappropriate immune responses • - Obstruction of urine flow • - Insufficient renal blood supply

27. Micturition • Urine stored in bladder is eliminated by micturition. • Urine in bladder stimulates stretch receptors. • Stimulated stretch receptors signal smooth muscle in bladder wall by parasympathetic neurons. Contraction of bladder pushes urine out of the body. • Micturition Reflex • Relaxation of external urethral sphincter muscle allowing urine to pass through urethra and out of the body • Under voluntary control but cannot be delayed indefinitely • Urinary Incontinence • Inability to prevent discharge of urine

29. Urinary Bladder and Its Innervation

30. Reflex and Voluntary Control of Mictrurition

31. There are 3 phases of vesicular pressure changes Initial 10 cm of H2O rise in pressure for 10-50 ml of urine collection Second phase last until the bladder volume is 400ml Third phase shows the sharp rise in the intravesicle pressure Micturition contractions begin to appear at a urine volume about 150 ml. Desire to void urine occurs when the bladder is full. Normal Cystogram

32. Abnormalities of micturition Atonic Bladder Caused by Destruction of Sensory Nerve Fibers: Micturition reflex cannot occur if the sensory nerve fibers from the bladder to the spinal cord are destroyed. Person loses bladder control. Instead of emptying periodically, the bladder fills to capacity and overflows a few drops at a time through the urethra. This is called overflow incontinence. A common cause of atonic bladder is crush injury to the sacral region of the spinal cord. Certain diseases can also

33. Automatic Bladder Caused by Spinal Cord damage above the sacral region. Typical micturition reflexes can still occur. They are no longer controlled by the brain. During the first few days to weeks the micturition reflexes are suppressed because “spinal shock” (sudden loss of facilitative impulses from the brain stem and cerebrum). Gradually typical micturition reflexes return; then, periodic (but unannounced) bladder emptying occurs. Some patients can still control urination in this condition by stimulating the skin (scratching or tickling) in the genital region, which sometimes elicits a micturition reflex.

34. Uninhibited Neurogenic Bladder Caused by lack of inhibitory signals from the brain. Which results in frequent and relatively uncontrolled micturition. From partial damage in the spinal cord or the brain stem that interrupts most of the inhibitory signals. Facilitative impulses passing continually down the cord -even a small quantity of urine elicits an uncontrollable micturition reflex, thereby promoting frequent urination.

35. REFERENCES • Human physiology by Lauralee Sherwood, seventh edition • Text book physiology by Guyton &Hall,11th edition • Text book of physiology by Linda S. Contanzo, third edition