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Control Of Body Fluid Osmolarity (Water Balance) Notes

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This is an extract of our Control Of Body Fluid Osmolarity (Water Balance) document, which we sell as part of our Renal System Notes collection written by the top tier of Bristol University students.

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Lecture 11 & 12 Control of Body Fluid Osmolarity (water balance)

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Why do we need to regulate fluid osmolarity and stay in water balance?
o Osmolarity= Conc. of solution expressed as (m)osmoles of solutes per litre of solution o Osmolarity of solution represents 'pulling power' it exerts in drawing water across o Depends on number of particles, not size o Osmolarity of plasma and ECF maintained at 285mOsm/L (+/- 4%) (N.B. not 300 mOsm/l) o Increased ECF osmolarity leads to withdrawal of water from cells=cell shrinkage o Reduced ECF leads to water entering cells=swelling o ECF osmolarity maintained constant despite wide variations in
? Water and salt intake
? Obligatory extra-renal losses of water and salt (e.g. sweat, expiration) How do we maintain constant ECF osmolarity?
o Stabilised by regulating body water (not salt) o Physiological control over both water intake (via thirst) and water output (urination) o Must compensate for
? Water generated via metabolism (not under physiological control)
? 'Obligatory' water loss via other routes (gut, skin, respiratory system. Either not under physiological control or is regulated for purposes other than water balance) Typical human water 'balance sheet' in 24hr period o Intake
? Dinking 1500ml
? Water in food 500ml
? Water from metabolism 400ml
? TOTAL 2400ml o Output
? Urine 1500ml (cannot be reduced <500ml)
? Respiration 400ml
? Skin 400ml
? Faeces 100ml
? TOTAL 2400ml Control of water excretion by ADH (VASOPRESSIN): an overview o Rate of water excretion set by ADH (vasopressin) o ADH=peptide hormone from posterior pituitary gland (PPG), below hypothalamus o Increases water permeability of cortical & medullary collecting ducts (possibly DCT) o Absence of ADH, walls of distal nephron impermeable to water o ADH binds V2 receptors in basolateral membranes of principle cells in distal parts of nephron o Up-regulates expression of AQUAPORINS which are then inserted into apical cell membrane

Water then moves osmotically from tubular fluid in distal nephron into surrounding interstitial and then blood Renal effects of ADH (vasopressin) o No ADH in blood
? Over hydration diuresis
? Cells that line cortical and medullary collecting duct are impermeable to water
? Na+ and Cl- do pass out but no H2O without ADH
? So urine more and more dilute as it passes down
? 80mOsm/L and 15-20ml/min (urine) o Maximal ADH in blood
? Dehydration Anti-Diuresis
? ADH binds to V2 receptors
? Inserts aquaporins into cortical & medullary collecting ducts
? Water will move until osmotic equilibrium is reached
? Urine very concentrated as max. osmolarity set up by renal medulla
? In diabetes

* Glucose adds to osmolarity of tubules so water stays in tubules and not reabsorbed=Diuresis Regulation of release of ADH from PPG o Mechanism
? Increased ECF osmolarity detected by osmoreceptors in hypothalamus, which shrink leading to increased frequency of nerve impulses along hypothalam0-hypophyseal tract
? Supraoptic & paraventricular nuclei (hypothalamus)=site of synthesis of ADH
? Increased frequency of nerve impulses causes secretion of the ADH from hypothalamo-hypophyseal nerve terminals
? ADH moves to PPG and is secreted from there o Level of ADH in blood controlled by negative feedback
? Increased blood osmolarity detected by hypothalamus osmoreceptors

* Raised blood osmolarity and low blood volumes also lead to sensation of thirst
? Increased release of ADH from PPG
? Insertion of aquaporins in distal nephron cell membranes
? Increased water permeability of distal nephron
? Increased reabsorption of water from distal nephron (under influence of medullary osmotic gradient) Effect of circulating blood volume in regulating ADH release o Decreased blood volume (hypovolaemia)
? Decreased venous return (volume receptors, B receptors in walls of great veins, right atrium. LOW PRESSURE side of circulation)
? Decreased BP (baroreceptors in carotids and aortic arch. HIGH PRESSURE) o Hypothalamus gets these signals leading to THIRST and INCREASED ADH Regulation of thirst o Sensation of thirst induced by
? Stimulation of hypothalamic osmoreceptors (via raised plasma osmolarity)

* Effect can be mimicked by injecting hypotonic saline
? Hypovolaemia detected by CV stretch receptors o

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