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SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
SSU Lecture 2
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SSU Lecture 2

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RDE SSU Lecture 2 …

RDE SSU Lecture 2
Renal electrolyte and water balance

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  • 1. RDE SSU 2 Water and Electrolyte Balance
  • 2. Aims & Content of this lecture
    • To continue providing you with a refresher in renal physiology that later lectures covering renal measurement and pathophysiology will build upon.
    • The role of antidiuretic hormone (ADH)
    • The renin-angiotensin-aldosterone system (RAAS)
    • Role of the kidney in volume regulation
    • Control of acid-base balance by the kidneys
    • Final review of how the renal system interacts with the cardiovascular and respiratory systems.
  • 3. ADH also needed to concentrate urine: how does it work?
    • Antidiuretic Hormone (ADH)/Arginine Vasopressin (AVP)
    • Increases permeability of collecting ducts to H 2 O by inserting H 2 O channels (Aquaporins).
    • Helps you make small amount of concentrated urine.
    • Reabsorption of H 2 O increase urea conc. in tubule, increasing its recycling effect.
    • ADH allows rapid, graded control of urine conc. – v. sensitive.
    • ADH released in response to plasma osmolality and ECF volume – osmoreceptors and baroreceptors.
  • 4. ADH (aka AVP)
    • Increased plasma osmolality stimulates osmoreceptors in the hypothalamus that trigger the release of ADH, which inhibits water excretion.
    • Increased osmolality stimulates a second group of osmoreceptors that trigger thirst, which promotes water intake.
    • Other factors also trigger ADH release e.g. decreased effective circulating volume, decreased BP, pregnancy, pain, morphine, nausea, congestive heart failure (CHF) (due to reduced ECV ).
    • CHF may cause such retention of H 2 O = hyponatremia.
    • Hyperaldosteronism = hypernatremia. Due to chronic volume expansion, where osmoreceptors become less sensitive to ADH, reducing ADH inappropriately.
  • 5. Renin-angiotensin-aldosterone axis
    • Principal factor controlling Ang II levels is renin release.
    • Decreased circulating volume stimulates renin release via:
      • Decreased BP (symp effects on JGA).
      • Decreased [NaCl] at macula densa (“NaCl sensor”)
      • Decreased renal perfusion pressure (“renal” baroreceptor)
  • 6. Angiotensin II – important actions
    • Stimulation of aldosterone release from adrenal cortex.
    • Vasoconstriction of renal and other systemic vessels.
    • Enhanced tubuloglomerular feedback – makes macula densa more sensitive.
    • Enhance Na-H exchanger and Na channel function to promote Na reabsorption.
    • Renal hypertrophy.
    • Stimulates thirst and ADH release by acting upon hypothalamus.
  • 7. Aldosterone
    • Aldosterone stimulates Na + reabsorption and K + excretion by the renal tubule.
    • Aldosterone exerts indirect negative feedback on RAAS by increasing ECV and by lowering plasma [K + ].
    • Really important in conserving Na + and water, but also really good at preventing massive swings in K + levels.
  • 8. Atrial Natriuretic Peptide (ANP)
    • ANP promotes natriuresis (loss of sodium).
    • Atrial myocytes synthesise, store and release ANP in response to stretch (low P volume sensor).
    • Major effect is renal vasodilatation. Increased blood flow = increased GFR.
    • Thus, more Na + reaches macula densa.
    • More Na + excreted.
    • May inhibit actions of renin, and generally opposes effects of angiotensin II.
  • 9. Feedback systems involved in osmolality control
  • 10. Comparison of systems controlling effective circulating volume and osmolality Water intake Brain: drinking behaviour Thirst Renal water excretion Short term : Blood pressure Long term : Na + excretion What is affected? Kidney Short term : heart, blood vessels Long term : Kidney Effector ADH RAAS, Symp NS, ADH, ANP Efferent Pathways Hypothalamic osmoreceptors Carotid sinus, aortic arch, renal afferent arteriole, atria Sensors Plasma Osmolality Effective Circulating Volume What is sensed?
  • 11. Control of effective circulating volume
    • Feedback control of effective circulating volume.
    • A low effective circulating volume triggers 4 parallel effector pathways that act on the kidney.
    • Either changes haemodynamics or changes Na + transport by renal tubule cells.
  • 12. ECF volume receptors
    • “ Central” vascular sensors
      • Low pressure (very important)
        • Cardiac atria
        • Pulmonary vasculature
      • High pressure (less important)
        • Carotid sinus
        • Aortic arch
        • Juxtaglomerular apparatus (renal afferent arteriole)
    • Sensors in the CNS (less important)
    • Sensors in the liver (less important)
    • N.B. Regulation of ECF volume = Regulation of body Na + . Thus, regulation of Na + also dependent upon baroreceptors.
  • 13. Another vital function of the kidneys: Acid-Base Balance
    • Kidneys really important for acid-base balance, along with respiratory system.
    • Again, another type of integrative physiology! (are you noticing a theme yet?)
    • Important because all biochemical processes must occur within an optimal pH window.
    • Prevent ACIDOSIS or ALKALOSIS.
    • Although the lungs excrete a large amount of CO 2 , a potential acid formed by metabolism, the kidneys are crucial for excreting non-volatile acids.
    • To maintain acid-base balance, kidney must not only reabsorb virtually all filtered HCO 3 - , but must also secrete into the urine the daily production of non-volatile acids.
  • 14. Sources of H+ gain and loss
    • H + Gain
      • CO 2 in blood (combine with H 2 O via carbonic anhydrase)
      • Nonvolatile acids from metabolism (e.g. lactic)
      • Loss of HCO 3 - in diarrhoea or non-gastric GI fluids
      • Loss of HCO 3 - in urine
    • H + Loss
      • Use of H + in metabolism of organic anions
      • Loss of H + in vomit
      • Loss of H + in urine
      • Hyperventilation (blow off CO 2 )
    • Loss of H + like gaining HCO 3 -
    • Loss of HCO 3 - like gaining H +
  • 15. HCO 3 - Reabsorption (main physiological buffer)
    • Kidneys alter/replenish H + by altering plasma [HCO 3 - ].
    • HCO 3 - filtered then practically all reabsorbed under normal conditions.
    • Prevents you gradually becoming acidotic because of metabolism. Gains = Losses, means maintain HOMEOSTASIS.
    • The secreted H + combines with filtered HCO 3 - in tubule to form CO 2 and H 2 O.
  • 16. Addition of new HCO 3 - to plasma by secretion of H +
    • When you use up filtered HCO 3 - in tubule and still have excess H + (acidosis), then you must combine H + with another buffer e.g. HPO 4 2- .
    • Unusual since lots of HCO 3 - in tubular fluid!
    • Gives net gain of HCO 3 - to plasma.
  • 17.
    • Another way of adding HCO 3 - to plasma by metabolising glutamine.
    • Takes long time though, so usually only occurs in chronic acidosis e.g. diabetes.
    Addition of new HCO 3 - to plasma by excretion of ammonium (NH 4 + )
  • 18. Normal urine & blood values:
    • Urine pH ~ 6.0
    • Blood pH = 7.4
    • Blood [HCO 3 - ] = 24 mM
    • Blood PCO 2 = 40 mmHg
    • Plasma osmolality = 285 mOsm/kg water
    • Urine osmolality (depends upon hydration status) = 600 mOsm/kg water (note that this can vary between 50-1200 depending on water intake etc.)
  • 19. Acid-base disorders
    • Remember, these can be either respiratory or metabolic in nature.
    • Respiratory ones can be chronic or acute; metabolic ones always chronic.
    • Only chronic ones cause marked change in HCO 3 - .
    • Renal and respiratory systems work together reflexly to compensate for one another.
  • 20. Final review of renal integration with respiratory and cardiovascular systems RENAL SYSTEM CARDIOVASCULAR SYSTEM RESPIRATORY SYSTEM Acid-base balance Gas exchange, ACE Effective circulating volume control, ECF osmolality, blood pressure All of these are constantly changing, trying to maintain HOMEOSTASIS!
  • 21. So, why do you need to know this?
    • Problems in one system are often only noticed by appearance of problems in another.
    • This is because of the integrated nature of these systems – they don’t operate in isolation.
    • Means we can sometimes compensate for problems in another system via reflexes, but also means that when disease progresses, lots of problems in several systems can begin to appear.
    • If we understand links between systems, we have more targets for drugs and other therapies to correct problems.
    • May also target actual cause of problem, rather than just worrying about the symptoms. Scientists think laterally – medics have a tendency just to stay inside their little window of expertise. PY3002 is all about getting you to think independently and laterally.
    • These three systems are probably the locations of most of the health-related problems you might encounter in whatever career you follow – regardless of whether you are a sports scientist or a physiologist.

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