L6 Physiology Countercurrent Multiplying System (PDF)
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Delta University Egypt
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This document covers the countercurrent multiplying system in the urinary system, including learning outcomes, descriptions of mechanisms for urine concentration and dilution, discussions on counter-current systems and vasa recta, and identification of urea cycles. It details different factors like fluid balance, osmolarity, and the role of vasopressin in urine concentration.
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The counter current multiplying and exchanging systems of loop of Henle and vasa recta respectively. Intended Learning Outcomes (ILOs) On completion of this lecture, the student will be able to: Describe mechanism of urine concentration and dilution. Discuss counter c...
The counter current multiplying and exchanging systems of loop of Henle and vasa recta respectively. Intended Learning Outcomes (ILOs) On completion of this lecture, the student will be able to: Describe mechanism of urine concentration and dilution. Discuss counter current system and vasa recta. Identify urea cycle. In fluid balance where osmolarity = 300mosmo/L Fluid is said to be isotonic If solutes in excess to water, osmolarity > 300mosmo/L Fluid is hypertonic (water deficit) If water in excess to solutes, osmolarity < 300mosmo/L Fluid is hypotonic Kidneys excrete urine of different concentrations according to body state to keep ECF osmolarity constant Kidneys have ability to excrete urine of different concentration 100 – 1200mosmo/L Kidneys are able to excrete this different concentration although water reabsorption is only through osmosis Kidneys change urine concentration from 100 – 1200mosm/l IF the body in: 1- fluid balance, 1ml/min excreted, isotonic = 300mosm/l 2- in overhydration, up to 25 ml/min excreted with osmolarity= 100mosm/l (overhydration) 3- in dehydration, urine can be decreased to 0.3 ml/min with osmolarity= 1200mosm/l (water deficit) Kidneys can produce different Urine concentrations Through its Vertical Osmotic Gradient and Vasopressin Dilution & concentration of urine 1) Vertical osmotic gradient 2) Change in permeability of DCT & CD Vasopressin Establishment Maintenance Counter current Urea Counter current Multiplier Recycling Exchange 60% 40% ( Vasa Recta ) 1) Vertical osmotic gradient Causes of Vertical osmotic gradient ( VOG ) Counter Current Urea Recycling System *Less role *Major cause *Produce gradient *Produce gradient in inner medulla through in outer medulla through *Passive Na transport *Active Na transport Counter current Two closely adjacent loops and Their fluid pass in opposite direction This arrangement is found in Loop of Henle of juxta medullary nephron and Vasa recta Counter current system Loop of Henle of Vasa Recta Juxta Medullary Nephron Create (establish) Maintains the VOG gradient through through Counter Current Counter Current Multiplication Exchange (Actively) (passively) Glomerulus Distal tubule Bowman’s capsule Proximal tubule COUNTER CURRENT Cortex MULTIPLIER Medulla Long loop Collecting tubule Collecting of Henle tubule COUNTER CURRENT MULTIPLICATION ESTABLISH THE VERTICAL OSMOTIC GRADIENT HOW ? TRANSPORT AND PERMEABILITY CHARACTERISTICS OF LOOP OF HENLE DESCENDING LOOP: 1- Highly permeable to water 2- impermeable to Na THIN ASCENDING LOOP: 1- Impermeable to water 2- Passively extrude Na THICK ASCENDING LOOP: 1- Impermeable to water 2- Actively extrude Na These transport and permeability characteristics create 200mosm. Concentration difference between thick loop and surroundings By counter current multiplication VOG created Lumen Distal tubular cell Interstitial fluid Medullary Peritubular interstitium capillary + K 2 Cl - 2 Cl - 2 Cl- Active Na pump Na+ Na+ can only Active transport Create gradient In osmolarity Tubular lumen K+ Na Na = 200 mosm/l + Diffusion Na Cells of thick ascending limb Active extrusion of sodium by thick ascending limb of loop of Henle of juxtamedullary nephron Urea that leaves PCT finally excreted in urine However Urea passively recycles between Lower part of collecting and Lower end of hairpin H2o Vasopressin increases urea concentration in inner medulla by: H2o o H2O reabsorption from collecting t. o permeability of inner collecting to urea INNER MEDULLA Urea Recycling Causes VOG In Inner Medulla Increase urea conc. In inner medulla Passive extrusion of Na from thin ascending loop How medulla can get blood supply without washing out this vertical osmotic gradient (1) Medulla has low blood supply Only 1-2 % of renal blood flow (2) Structure of the blood capillaries supplying the medulla [vasa recta] Vasa recta Maintains Vertical osmotic gradient Vasa recta Thus can supply blood and remove waste and reabsorbed substances (through bulk flow, reabsorbing force) With maintaining Vertical osmotic gradient Summary to the factors that build up medullary VOG Active Na transport – by thick ascending creates 200 mosm/l. Counter current multiplier – establish the VOG. Passive diffusion of urea from inner medullary collecting ducts & the accompanied passive extrusion of Na from thin ascending limb – increases osmolarity of the inner medulla. Glomerulus Distal tubule Bowman’s capsule COUNTER CURRENT Proximal tubule MULTIPLIER (establish gradient) Cortex 300 300 Medulla 600 600 Collecting tubule outer 900 900 Long loop Collecting of Henle tubule 1200 1200 1200 1200 inner From To vein efferent arteriole Cortex of kidney Medulla of kidney Vasa recta (utilization of VOG) 2) Change permeability of distal segment “Vasopressin Role” Volume 25 ml/min (20% of GFR) Osmolarity 100 mosm/l (hypotonic) Distal & Collecting tubules are impermeable to H2O except in the presence of Vasopressin Tubular Peritubular lumen capillary filtrate Distal tubular cell plasma Increases permeability of luminal membrane to H2O by inserting new Water water channels channel The membrane permeability is dependent on level of vasopressin secreted More vasopressin more channels inserted more permeability to H2o In Water Deficit Vasopressin secretion is stimulated, level of vasopressin secretion // degree of water deficit Maximum vasopressin secretion causes maximum permeability of membrane of distal and collecting tubules Fluid in DCT osmolarity will be = 300 mosm/l Osmolarity of fluid descending in collecting will progressively increases, reaching maximum 1200 mosm/l Excreted urine will be 1200mosm/l and vol.=0.3 ml/min (=500 ml/day) Maximum vasopressin secretion cannot stop urine flow completely In Water Excess Inhibition of vasopressin secretion, distal & collecting tubules are impermeable to water In absence of vasopressin 20% of water reaching DCT is excreted (25 ml/min). Excreted fluid will be diluted (hypotonic) Because fluid leaving loop of Henle is diluted (100mosm/l). What is the main function of the counter- current multiplication system in the kidney? 1.Removal of urea from the proximal tubule 2.Establishment of the vertical osmotic gradient in the medulla 3.Filtration of plasma in the glomerulus 4.Maintenance of blood pH 5.Active reabsorption of water in the descending limb of the loop of Henle Which part of the nephron is impermeable to water but actively extrudes sodium? 1.Descending limb of the loop of Henle 2.Thin ascending limb of the loop of Henle 3.Thick ascending limb of the loop of Henle 4.Proximal convoluted tubule 5.Collecting duct What is the osmolarity of urine during a state of overhydration? 1.300 mosm/L 2.100 mosm/L 3.1200 mosm/L 4.600 mosm/L 5.200 mosm/L Which of the following statements about urea recycling is correct? 1.It occurs in the proximal convoluted tubule only. 2.It increases urea concentration in the cortex of the kidney. 3.It contributes to the osmolarity of the inner medulla. 4.It depends on active urea transport in the ascending limb. 5.It is regulated by aldosterone. Which of the following factors is responsible for establishing the vertical osmotic gradient (VOG) in the kidney? 1.Active sodium transport in the thick ascending limb of the loop of Henle 2.Passive diffusion of sodium in the descending limb of the loop of Henle 3.Active urea transport in the proximal tubule 4.Counter-current exchange in the vasa recta 5.Secretion of aldosterone References Ganong, W.F.: Review of medical physiology, 23 th ed. New York, Mc Graw- Hill Co, 2011. P654:657. Gyton, A.A. and Hall, J.E.: Text book of medical physiology, 12 th ed. Philadelphia, Saunders Co., 2011.P 345:360 Handbook of the Physiology department, Faculty of medicine for girls, Al-Azhar university, P 49:55