Concentration and Dilution of Urine Flashcards
Reabsorption of water in the nephron
Filtrate: 180L/day. Urine is 1% of filtrate
65-70% in PCT not regulated
20% in Loop of Henle, not regulated
Collecting duct regulated water absoption
Explain how solute conentration alters urine volume
The maximum urine osmolality (concentration of solutes) is 1200 mosmol.
If the concentration of solutes is increased above this, then the kidneys exrete this by producing more urine.
High levels of solute cause a diuresis even if high levels of ADH are present
How is the extracellular fluid involved in fluid balance?
ECF volume controls the blood pressure
ECF osmolarity maintains cell volume
Kidneys regulate fluid balance by altering the plasma to regulate body fluid volume and osmolarity.
How does the kidney regulate the concentration of urea in the interstitial fluid?
50% of the urea that is filtered by the glomerulus is reabsorbed by the proximal convoluted tubule. The rest remains in the nephron, which is impermeable to urea. The concentration of urea increases because water is reabsorbed.
When it reaches the medullary collecting duct 70% of the urea in the collecting duct is reabsorbed and secreted into the loop of Henle. Urea re-circulates in the nephron.10% of the filtered load goes into the medulla, 40% is excreted. This creates a flow of urea that stops it precipitating in the medullary tissue.
Factors regulating the concentration of urine by the nephron
Length of the loop of Henle
Rate of NaCl reabsorption in the thick ascending limb (can be altered by GFR, diuretics, absorption in PCT)
Luminal flow rate through the loop (higher rate, less concentrated urine, counter-current flow less effective)
Protein content of the diet (increases concentration)
Osmotic permeability of the collecting duct (e.g. ADH)
Medullar blood flow (high flow rate washes out medullary solutes)
Name three physiological factors that stimulate ADH release
Increased plasma osmolality
Extracellular volume reduction
Thirst
Nausea (preparation for expected vomiting and fluid loss)
Drugs (nicotine, morphine, barbiturates)
Angiotensin II
Functions of ADH
Reduce water excretion
Stimulate vasoconstriction
Synthesis of ADH
The posterior pituitary is connected to specific hypothalmic nucle neuranatomically.
ADH is synthesied in the supraoptic and paraventricular nuclei in the anterior hypothalamus and is transported along the axon and stored in the posterior pituitary.
ADH is packaged into storage granules and is released by exocytosis. Plasma half life is 10-15mins
ADH and oxytocin have a similar sequence
Action of ADH
ADH stimulates V2 receptors allows the collecting ducts to become permeable to water via the migration vesicles containing aquaporin-2 water channels which fuse with the apical membrane. This allows reabsorption fluid. ADH binding to V2 receptors also stimulates the synthesis of more aquaporins.
ADH reduces diuresis and results in overall retention of water. At high concentrations vasopressin causes vasoconstriction via V1R in vascular tissue.
Types of aquaporins
Produce tissure-specific responses to ADH
AQP1: widely distributed
AQP2: collecting duct (apical membrane), regulated by ADH
AQP3 and AQP4: collecting duct (basolateral membrane) allows H2O reabsorbed from the lumen to enter the interstitium
AQP5: primarily non-renal (brain, lungs)
SIADH
Syndrome of inappropriate ADH secretion.
Patients wtih SIADH have impaired water excretion and hyponatremia caused by the presence of ADH.
The release of ANP and aldosterone is not impaired, so Na+ remains intact.
causes of SIADH
CNS - lesions, inflammation, damage/trauma
Pulmonary: TB, pneumonia, respiratory failure, COPD, tumour
Drug induced: stimulates ADH release, act on the kidney e.g. narcotics, oxytocin, nicotine
Diabetes Insipidus
Inability to reabsorb water from the distal part of the nephron due to the failure of secretion or action of ADH.
Symptoms are: polydipsia, Polyuria, Dilute urine
Causes can be neurogenic: impaired ADH synthesis or secretion by the hypothalamus. ADH can be administered
Nephrogenic: failure of the kidneys tor espond to circulating ADH, due to mutation of the receptors, pyelonephritis, polycystic kidneys or drugs.
Control of ADH release
A rise is plasma osmolality triggers ADH release. Increased plasma osmolarity causes cellular dehydration. This is detected by osmoreceptors in the hypothalamus.
Action potentials in the neurons from the hypothalamus depolarise the axon membrane resulting in Ca2+ influx, fusion of secretory granules with the axon membrane and release of ADH (and neurophysis) into the blood stream.
Extracellular dehydration caused by low fluid volume is detected by peripheral receptors e.g. stretch receptors in the atrium, pulmory veins, carotid sinus, afferent arterioles detect a decrease in strech/pressure which stimulates ADH release.
Name for factors that inhibit ADH release
Low plasma osmolality
Alcohol
Cold
Emotional stress
(All cause fluid loss)
Describe the role of the vasa recta in water reabsorption of the kidney
Vasa recta are long thin walled blood vessels derived from efferent arterioles that run in parallel to the loops of Henle. They act to maintain the main osmotic gradient of the medulla and remove ions and water that has been reabsorbed. Low blood flow helps maintain osmolality.
Blood entering the vasa recta is isotonic with the plasma. Walls of the descending limb are permable to salts and water so as blood passes through the medulla water moves out and solutes move in until the osmolality is equal to the interstitum.
As the blood returns towards the cortex some solutes are reabsorbed and water enters the ascending lumb so blood leaving the vasa recta is only slightly hyperosmotic to the plasma.
