Ch 20 Integrative Physiology II Fluid & Electrolyte Balance

1. Ch 20 Integrative Physiology IIFluid & Electrolyte Balance Objectives • Explain homeostasis of • Water Balance (ECF/ICF volumes) • Electrolyte Balance (osmolarity), • Acid-Base Balance (pH)

2. Kidneys maintain H2O balance by regulating urine concentration • Daily H2O intake balanced by H2O excretion • Kidneys react to changes in osmolarity, volume, and blood pressure Fig 20-2 Fig 20-1 Urinary System: Early Filtrate Processing CD Animation

3. H2O excretion in kidneys controlled primarily by vasopressin (= antidiuretic hormone = ADH) ADH  Fast response ! Fig 20-1

4. Nephron Recycling: Overview At beginning of LOH: ~ 65 % of H2O & solutes are reabsorbed (filtrate isosmotic with IF) Urine concentration can vary between 50 – 1200 mOsM How does Nephron Establish Urine Concentration ?

5. Urine Concentration Established by LOH and CD  reabsorption of varying amounts of H2O and Na+ Key player: ADH(= Vasopressin) Fig 20-4

6. Fig 20-4

7. ADH - Vasopressin Released from? when? Controls water permeability of last section of DCT and all of CD Regulates AQP2 channel 2nd messenger mechanism transduces ADH signal to cell interior  Insertion of water pores in apical membrane Fig 20-6

8. ADH Mechanism Fig 20-6

9. Regulation of ADH ADH release regulated via • ECF osmolarity • Blood pressure and volume Diabetes insipidus – central vs. nephrogenic Nocturnal enuresis Fig 20-7

10. ADH Regulation Fig 20-7

11. Review: Concentrated vs. Dilute Urine In presence of ADH: Insertion of H2O pores At maximal H2O permeability: Net H2O movement stops at equilibrium Maximum osmolarity of urine? No ADH: DCT & CD impermeable to H2O Osmolarity can plunge to ~ 50 mOsm Fig 20-5

12. ADH No ADH Fig 20-5

13. LOH:Countercurrent Multiplier leads to Hyperosmotic IF in medulla Hyposmotic fluid leaving LOH

14. Na+ Balance and ECF Volume • [Na+] affects plasma & ECF osmolarity (Normal [Na+]ECF ~ 140 mosmol) • [Na+] affects blood pressure & ECF volume (?) Aldosterone regulates Na+ (and K+) excretion in last 1/3 of DCT and CD • Type of hormone? Where produced? Type of mechanism? •  Aldosterone secretion   Na+ absorption Fig 20-13

15. Fig 20-13 Aldosterone Mechanism Here (unlike normally) H2O does not necessarily follow Na+ absorption. This only happens in presence of . . . Na+/K+ ATPase activity   K+ secretion

16. Acid–Base Balance Fig 20-19 • Normal blood pH ? • Enzymes & NS very sensitive to pH changes • Kidneys have K+/H+ antiporter • Importance of hyperkalemia and hypokalemia • Acidosis vs. alkalosis

17. Acidosis Respiratory acidosisdue to alveolar hypoventilation (accumulation of CO2) Possible causes: Respiratory depression, increased airway resistance (?), impaired gas exchange (emphysema, fibrosis, muscular dystrophy, pneumonia) Metabolic acidosisdue to gain of fixed acid or loss of bicarbonate Possible causes: lactic acidosis, ketoacidosis, diarrhea Buffer capabilities exceeded once pH change appears in plasma. Options for compensation?

18. Body deals with pH changes by 3 mechanisms Buffers 1st defense, immediate response Ventilation 2nd line of defense, can handle ~ 75% of most pH disturbances Renal regulation of H+ & HCO3- final defense, slow but very effective Fig 20-21

19. Renal Compensation for Acidosis Fig 20-21

20. Alkalosis much rarer Respiratory alkalosisdue to alveolar hyperventilation in the absence of increased metabolic CO2 production Possible causes: Anxiety with hysterical hyperventilation, excessive artificial ventilation, aspirin toxicity, fever, high altitude Compensation? Metabolic alkalosisdue to loss of H+ ions or shift of H+ into the intracellular space. Possible causes: Vomiting or nasogastric (NG) suction; antacid overdose Compensation? Buffer capabilities exceeded once pH change appears in plasma. the end