Ch 20 Integrative Physiology II

Fluid & Electrolyte Balance

Explain homeostasis ofExplain homeostasis of

1.1. Water Balance Water Balance (ECF/ICF volumes)(ECF/ICF volumes)

2. Electrolyte Balance (osmolarity),

3. Acid-Base Balance (pH)

ObjectivesObjectives

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 20-1

CD AnimationUrinary System: Early Filtrate Processing

Fig 20-2

H2O excretion in kidneys controlled

primarily by vasopressin

(= antidiuretic hormone = ADH)

Fast response !

ADH

Fig 20-1

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 ?

Urine ConcentrationEstablished by LOH and CD

reabsorption of varying amounts of H2O and Na+

Key player: ADH (= Vasopressin)

Fig 20-4

Fig 20-4

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

ADH MechanismADH Mechanism

Fig 20-6

Regulation of ADHADH release regulated via 1. ECF osmolarity 2. Blood pressure and volume

Diabetes insipidus – central vs. nephrogenic

Nocturnal enuresis

Fig 20-7

ADH RegulationADH Regulation

Fig 20-7

Concentrated vs. Dilute UrineIn 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

Review:

Fig 20-5

Fig 20-5 ADH No ADH

LOH:Countercurrent

Multiplier

leads to

Hyperosmotic IF in medulla

Hyposmotic fluid leaving LOH

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

Aldosterone MechanismAldosterone Mechanism

Na+/K+ ATPase activity K+ secretion

Here (unlike normally) H2O does not necessarily follow Na+ absorption. This only happens in presence of . . .

Fig 20-13

Acid–Base Balance• Normal blood pH ?

• Enzymes & NS very sensitive to pH changes

• Kidneys have K+/H+ antiporter

• Importance of hyperkalemia and hypokalemia

• Acidosis vs. alkalosis

Fig 20-19

AcidosisRespiratory acidosis due to alveolar

hypoventilation (accumulation of CO2)Possible causes: Respiratory depression, increased

airway resistance (?), impaired gas exchange (emphysema, fibrosis, muscular dystrophy, pneumonia)

Metabolic acidosis due 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?

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 effectiveFig 20-21

Renal Compensation for AcidosisRenal Compensation for Acidosis

Fig 20-21

Alkalosis much rarer

Respiratory alkalosis due 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 alkalosis due 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.