Presentation on theme: "Regulation of Extracellular Fluid Osmolarity and Sodium Concentration"— Presentation transcript:
1Regulation of Extracellular Fluid Osmolarity and Sodium Concentration
2Excretion of excessive water by forming a dilute urine The kidneys can excrete urine with an osmolarity as low as 50 mOsm/L (1/6 of normal urine osmolarity)Conversely, when there is a deficit of water and extracellular fluid osmolarity is high, the kidney can excrete a urine with osmolarity as high as mOsm/LRole of anti-diuretic hormone (Vasopressin) in concentrating urine
4Generating a dilute urine from: Guyton, AG & Hall, JE, Medical Physiology (10th Ed.), 2000, Chp. 28.A dilute urine results from the reabsorption of salt from tubule segmentsimpermeable to H2O.
5Tubular Fluid Becomes Dilute in the Ascending Loop of Henle
6Excretion of Concentrated Urine Ability of the kidney to form a more concentrated urine is essential for survivalIt is achieved by increased water reabsorption and increased solute excretionObligatory urine volumeA normal adult must excrete about 600 mOsm of solutes per dayIf the maximal urine concentration ability is 1200 mOsm/L, the minimal volume of urine that must be excreted:600 mOsm L/ 1200 mOsm L = 0.5 L/ Day
7Requirements for excreting a concentrated urine High ADH levelsHyperosmotic renal medulla which provides the osmotic gradient necessary for water reabsorption to occur in the presence of high levels of ADH
8Generating a concentrated urine A concentrated urine results from the reabsorption of H2O (by osmosis)from tubule segments that are exposed to a hyperosmotic interstitium.
9Requirements for excreting a concentrated urine Major factors that contribute to the buildup of solute concentration in the renal medulla:Active transport of Na ions and co-transport of K, Cl and other ions out of the thick portion of HenleActive transport of ions from the collecting ducts into the medullary interstitiumFacilitated diffusion of urea from the medullary collecting ducts into the medullary interstitiumDiffusion of only small amounts of water from the medullary tubules into the medullary interstitium
10Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium
11Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium Countercurrent multiplicationBetween ascending and descending limbs of loopCreates osmotic gradient in medullaFacilitates reabsorption of water and solutes before the DCTPermits passive reabsorption of water from tubular fluid
12Role of distal tubule and collecting ducts in excreting a concentrated urine
13Urea Contributes to Hyperosmotic Renal Medullary Interstitum and to a Concentrated Urine
14Preservation of Hyperosmolarity by Vasa Recta 1) Medullary blood flow is low2) The vasa recta serves as countercurrent exchangersThe vasa recta does not create the hyperosmolarity, but they do prevent it from being washed away
15The vasa recta The vasa recta are hairpin- shaped vessels that run parallel to the loop of Henle.
18Disorders of Urinary Concentrating Ability 1) Inappropriate secretion of ADH2) Impairement of countercurrent mechanism3) Inability of the distal tubule, collecting tubule and collecting ducts to respond to ADHFailure to produce ADH (Central diabetes insipidus)Inability of the kidneys to respond to ADH (Nephrogenic diabetes insipidus)
20Control of Extracellular Fluid Osmolarity and Na Concentration Osmoreceptor – ADH feedback system
21ADH Synthesis in Supraoptic and Paraventricular Nuclei of the Hypothalamus and ADH release from the posterior pituitary
22Decreased arterial pressure and / or blood volume Cardiovascular reflex stimulation of ADH release by decreased Arterial Pressure and/or decreased blood volumeDecreased arterial pressure and / or blood volumeArterial baroreceptor reflexesCardiopulmonary reflexesIncrease ADHDecrease ADH↑ Plasma osmolarity↓ Plasma osmolarity↓ Blood volume↑ Blood volume↓ Blood pressure↑ Blood pressureNauseaHypoxiaDrugs: Morphine Alcohol Nicotine Clonidine (antihypertensive drug) Cyclophosphamide Haloperidol (dopamine blocker)
23Role of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration CNS centers for thirst – hypothalamus – anteroventral wall of the 3rd ventricleStimuli for thirst: increased extracellular fluid osmolaritySalt-apetite mechanism for controlling extracellular fluid Na concentration and volumeThere are two primary stimuli to increase salt apetite:Decreased extracellular fluid Na concentrationDecreased blood volume or blood pressure associated with circulatory insufficiency
24Control of Extracellular Fluid Sodium Concentration: ADH and Thirst