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2013-11-24 06:37:55

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  1. mechanism of Na RE-ABSORPTION in proximal tubule
    • Proximal Tubule :(acetazolamide inhibits)
    • Na/H antiporter
    • Na/S symporter
    • Transcellular transport
  2. mechanism of Na RE-ABSORPTION in loop of henle
    • loop of henle (furosemide inhibit)
    • Na/K/2Cl cotransporter/symport
    • transcellular transport
  3. mechanism of Na RE-ABSORPTION in distal nephron
    • distal tubule:(thiazide inhibits)
    • Na/Cl symporter
    • Na channel
  4. water househld
    • Water intake - 2100-3400 ml/day
    • Fluid intake 1000-2000 ml/day
    • Water content of foodstuffs 800-1000 ml/day
    • Oxidative water 300-400 ml/day

    • Water output-  2100-3400 ml/day
    • Insensible perspiration 800-1000 ml/day
    • sensible perspiration, sweating 200 ml/day
    • Stool 100-200 ml/day
    • Urine 1000-2000 ml/day

    Minimal urine output 500-600 ml/day (650 mosm solute/day).
  5. physiology of thirst
    • dryness of the mouth 
    • angiotensin 2 
    • hypthalamic osmoreceptors
  6. control of water intake
    • hyperosmosis
    • hypovolaemy
    • 1)water reabsorption from the collecting duct through aquaporin 2 water channels ( v2/cAMP) receptors in the basolateral
    • 2)v1/itp - ca vasoconstrictor effect (v1 receptors are on blood vessels mechanism is ca-Ip3)
    • 3)v3 receptor in the ACTH -Adrenocorticotropic hormone - producing neurons of the anterior petuitary gland
  8. vasopressin (wekipedia )
    Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body's retention of water by acting to increase water absorption in the collecting ducts of the kidney nephron.

    It is derived from a preprohormone precursor that is synthesized in the hypothalamusand stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the bloodstream. 

    Vasopressin is a peptide hormone that increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.[3] It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood.
  9. aqua porin
    Aquaporins allow water to move down their osmotic gradient and out of the nephron, increasing the amount of water re-absorbed from the filtrate (forming urine) back into the bloodstream.
  10. vasopressin in the kidney
    • Vasopressin has two main effects by which it contributes to increased urine osmolarity (increased concentration) and decreased water excretion:
    • Increasing the water permeability of distal tubule and collecting duct cells in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis. This occurs through insertion of water channels (Aquaporin-2) into the apical membrane of distal tubule and collecting duct epithelial cells. 

    • V2 receptors, which are G protein-coupled receptors on the basolateral plasma membrane of the epithelial cells
    • Vasopressin 2/ITP also increases the concentration of calcium in the collecting duct cells, by episodic release from intracellular stores.
    • Vasopressin, acting through cAMP, also increases transcription of the aquaporin-2 gene, thus increasing the total number of aquaporin-2 molecules in collecting duct cells.Cyclic-AMP activates protein kinase A (PKA) by binding to its regulatory subunits and allowing them to detach from the catalytic subunits. Detachment exposes the catalytic site in the enzyme, allowing it to add phosphate groups to proteins (including the aquaporin-2 protein), which alters their functions.Increasing permeability of the inner medullary portion of the collecting duct to urea by regulating the cell surface expression of urea transporters,[5] which facilitates its reabsorption into the medullary interstitium as it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct.
  11. ADH
    • presence of ADH the water PERMEABILY of the whole collecting duct and the urea permiabilty of its PAPILLARY PART GREATLY INCREASIS
    • 3.collecting duct is relatively impermiable to water and urea in the absence of ADH
    • 4.basolateral v2 receptor adrenylate cyclase cAMP
    •  5.hormone of posterior pituitary gland
    • 6.produced by supraoptic nucleus of hypothalamus 
    • 7.oligopeptide containing 8 amino acids 
    • 8.Human ADH is charecterized by ARGENINE VASOPRESSIN(AVP)
    • 9/IN HIGHER doses it causes vasoconstriction through V1 RECEPTORS

  12. apical
    b/w the lumen of the tubule and the epithelium of the collecting duct
  13. basolater
    b/w the vasa recta and the epithelium of the collecting duct
  14. renal papilla 
    is the location where the medullary pyramids empty urine into the minor calyx in the kidney.
  15. in the absence of the ADH or V2 ADH receptor:
    diabetes insipidus :
    • 1.osmolarity of fluid that leaves the collecting duct is 70 mom/kg (50 mosm/kg urea and 20 mosm/kg electrolyte)--->increase plasma osmolarity
    • 2.  15% of the filtered water will be EXRETED (max.26 liter/day)---> decrease the blood volume

  16. ADH secretion increased by
    • Increased by  
    • 1. High osmolarity of the blood
    • 2. Hypovolemia (inhibits ANP secretion)
    • 3. Standing ↓ ANP ↓
    • 4. venous stasis
    • 5. pain, exercise
  17. ADH secretion decreased by
    • decreased by:
    • 1. low blood osmolarity
    • 2.hypervolemia
    • 3.lying in horisontal position ( increase ANP)
    • 4.ALCOHOL
  18. cc and dilution of the urine
    • depending on the need of the body the kidney can produce :
    • highly concentrated (to 1.2 mosm/l)
    • strongly diluted urin (to 50 mosm/l)
  19. influincing the urine cc:
    • 1.Length of Henle loops
    • 2.Percentage of long-looped nephrons compared to short-looped ones
    • 3.Urea
    • 4.Flow through Henle-loop and collecting duct
    • 5.Blood-flow through vasa recta
    • 6.Prostaglandines (PGE2, PGD2)
  20. cc and dilution of the urine 
    medullary gradient is due to :

    300 mosm/kg - 1200 mosm/kg 

    medullary cc. originates from the countercurrent multiplication mechanism

    •  horisontal gradientactive Na reabsorption in ascending THICK segment of loop of henle 
    • vertical gradient-countercurrent 
    • fluid movement in the descending and ascending segment of loop of henle

    loop diuretics f.e fursemide--->abolishes medullary gradient 

    a countercurrent multiplier system is a mechanism that expends energy to create a concentration gradient.It is found widely in nature and especially in mammalian organs. For example, it can refer to the process that is underlying the process of urine concentration, that is, the production of hyperosmotic urine by the mammalian kidney
  21. hyperosmotic urine= concentrated urine
    • urine cc. > blood osmolarity
    • ADH level is high in this situation (water deprivation , hemorrhage,SIADH)
  22. urea
    • 1.50% of the filtrated urea is REABSORBED PASSIVELY in proximal tubule
    • 2. 1)distal tubule 2)cortical collecting ducts 3)outer medullary collectiong duct --> impermiable to urea,no urea is reabsorbed there
    • 3. ADH icreases urea permiability of the inner medullary collecting duct ,UREA IS REABSORED HERE, which contributes to UREA RECYCLING IN THE INNER MEDULLA , and develop corticopapillary osmotic gradient 
    • 4.urea excretion varies with urine flow rate

  23. low urine flow rate
    • high levels of water reabsorption (low urine flow rate)
    • 2.there is greater urea reabsorption 
    • 3.decreased urea excretion
  24. motor of concentrating of the urine (hyperosmolar renal medulla)
    is electrolyte transport in the loop of henle

  25. loop of henle and osmolarity
    1.most important rule of loop of henle is the building of HYPEROSMOLAR RENAL MEDULLA

    • 2.ASCENDING THICK SEGMENT--> reabsorbs actively Na and Cl (practically without water reabsorption)

    The loop form structure of Vasa Recta prevents the dilution of renal medulla. Countercurrent system does not allow the quickly transport of 1.NaCl  2.urea.

    • The hyperosmolarity and the medullar gratient would be washed out quickly, if the blod flow and the form of blood wessels would be conventional.
  27. CC. of urin will be inhibited through
    • 1.Loop diuretics (Inhibition of Na+,K+,2Cl--Symporters)-(fursoemide -may zeidan) 
    • 2.Potassium deficit (inhibits the Na+,K+,2Cl--symporter)-
    • 3.Hyperkalcaemia (Decreasing the permeability of tight junctions, Ca2+-receptors inhibiting the Na+,K+,2Cl--symporter)-
    • 4.Proteipoor nutrition-
    • 5.Renal inflammation (Dilatation of Vasa recta)-
    • 6.Increase of blood pressure-
    • 7.Osmotic diuresis -increase urination (filtration of no or partial resorbable osmotic active substances)
    • 8. Diabetes insipidus
  28. daily urine amount
  29. specific gravity
    1001-1030 g/Liter
  30. osmolarity of urine
    70 - 1200 mosm/kg
  31. osmotic clearance
    urinary osmolarity*velocity of urine flow / plasma osmolarity
  32. free water clearance
    v(urine flow)-sum of osmolar (Cosm=plasma + urine osmolarity)
  33. salt household
    • Na+ intake:
    • 1.Na+ content of drinks and food between 10 and 600 mmol
    • 2.Na+ (100-400mmol/day in general ).
    • 3.No physiological mechanism of Na+ intake :
    • Na+ loss:
    • Sweat
    • Stool
    • Urine (100-400 mmol/day).

    Regulation of salt household Through salt loss.
  34. isosmosis receptors
    • Osmoreceptors (1%)
    • ,baroreceptors.
    • Volume receptors (10 %)
  35. effector mechanism (regulation of Na househld)
    • 1.GFR 
    • 2.renin angiotensin aldosteron system 
    • Adrenal cortex glomerular zone (mineralocorticoid)Na+ and K+ion exchange in the distal tubule and collecting duct
    • 3.third factor

  36. renin angiotensin aldosteron system - the structures involved
    • 1)A iuxtaglomerular apparatus
    • 1.myoepithel cells of vas afferents
    • 2.macula densa in distal tubulus
    • 3.mesangial connective tissue

    2)Renin ( 66500 d)

    • 3).angiotensinogén (alfa2-globulin, liver)
    • Angiotensine I (10 amino acid (ACE, angiotensine converting enzyme)
    • Angiotensine II (8 amino acid)
    • Angiotensine III
  37. Angiotenzin II effects
    1. Blood pressure vasoconstrictor (systolic and diastolic RR increases

    2/ salt loss:RBF, GFR decreases,Direct inhibition of Na+ tubular reabsorption,Dominating salt retention.

    3/ Aldosteron

    4/ dypsogenic effect
  38. renin secretion decreased
    • 1. prostaglandines ( PGE2, PGD2, PGI2)
    • 2. atrial natriuretikus factor (ANF) Renal hypertension (experimentalis renalis hypertonia)
    • 3. “Third factor” effect 
    • 1. A syimpathic stimulation,
    • 2. An angiotensin II
    • 3. An ANF
    • 4. A peritubularis capillaries
  39. Renin secretion increases
    • 1. decreased renal blood flow (dicreased blood pressure)
    • 2. amount and chemical composition-NaCl) of tubular fluid at macula densa
    • 3. stimulation of renalis sympasathic nerve
    • 4. extracellular hypovolemia (bleeding)
    • 5.internal tissue pressure dicrease

  40. factors increase ALDOSTERONE SECRETION
    • 1.ANGIOTENSIN 2 
    • 2.dicrease plasma Na  
    • 3.increase plasma k
    • 4.DECREASE 
    • 4.ACTH 
    • Adrenocorticotropic hormone (ACTH), also known as corticotropin, is a polypeptide tropic hormone produced and secreted by the anterior pituitary gland. It is an important component of the hypothalamic-pituitary-adrenal axisand is often produced in response to biological stress (along with its precursorcorticotropin-releasing hormone from the hypothalamus). Its principal effects are increased production and release of corticosteroids.
  41. ANF atrial natriuretic factor
    • right atrium
    • 28 amino acids (2800 - 13000 dalton)
    • 126 amino acid precursor (atropeptinogen
  42. ANF secreted 
    • 1. increase atrial stretch (hypervolemia)
    • 2.adrenaline 
    • 3.Ach
    • 4.ADH
    • 1.vasodilation
    • 2.increase the GFR (dilation of the afferent arteriole )
    • 4.inhibition of ADH
    • 5.decrease Aldosteron secretion 
    • 6.natriuresis annd water diuresis 
    • 7.decreased cardiac output
    • 8.blood pressure decrease
  44. diuretics which inhibits Na reabsorption in tubulary system 
    • 1.carbon anhydraze inhibitor
    • 2.loop diuretics
    • 3.thiazide 
    • 4.AT2 antagonist (lostran)
    • 5.aldosteron antagonist (spironolacton)