Physiology 1, Fall 2008, LPC

Chapter 20- Fluid & Electrolyte Balance

I – Fluid & Electrolyte Homeostasis

Water follows salts, can lead to swelling or dehydration which impair cell function
[K+] affects cardiac & muscle function (nerves & muscles)
[Ca++], [H+], [HCO3-] affect many body functions

blood volume affects blood pressure; coordinated by respiratory, cardiovascular, renal systems and behavioral responses

II – Water Balance

H2O enters body via digestive tract & as metabolic by-product
H2O leaves body via urine and (insensible) sweating, exhalation
Kidneys conserve H2O. If no extra H2O, no urine formation.
Loop of Henle & Collecting Duct determine urine concentration

Urine concentration determined by amounts of H2O & Na+ reabsorbed in distal nephron
Na+, K+, Cl- transported out of tubule lumen or thick portion of ascending limb of the loop. Surface of cells facing tubule lumen impermeable to H2O
Concentration of fluid in collecting duct determined by H2O permeability of epithelial cells in distal tubule
H2O reabsorption controllable in collecting duct also

Vasopressin (ADH, antidiuretic hormone) moves water pores to cells of collecting duct to allow H2O to go into renal medulla

no vasopressin, no water movement
response graded, not all-or- none
High osmolarity, low blood volume, and/or low blood pressure -> vasopressin synthesis & release -> increased H2O reabsorption

Countercurrent mechanisms

Two exchanging structures very close together so can exchange heat or materials easily

Extremities of animals living in cold – warmest blood closest to body and reheats blood as it returns from cold. Prevents heat from going out to cold environment.

Nephron

Ascending limb pumps Na+, K+ and Cl- into interstitial fluid, -> urine more dilute
Na+, K+, Cl- from interstitial fluid goes into vasa recta, blood becomes more concentrated as it descends loop.  Blood circulation forces increased salt concentration towards renal medulla.
High salt concentration in medulla attracts water from dilute (& becoming more concentrated) urine

Active reabsorption of ions into interstitial fluid around thick ascending limb creates a dilute filtrate.
Close anatomical association of loop of Henle and peritubular capillaries allows vasa recta to absorb water via concentration gradient.

Urea contributes to high osmolarity of medullary interstitium

III – Sodium Balance & ECF Volume

ingestion of salt without fluid -> increased osmolarity

vasopressin -> kidneys conserve H2O
thirst -> increased H2O ->increased ECF -> kidneys excrete salt & water increased blood pressure –> cardiovascular response

Blood pressure controls aldosterone secretion

Aldosterone -> distal tubules & collecting ducts to more Na+ reabsorption, & K+ secretion. Increases salt content of blood
Aldosterone binds cytoplasmic receptor, -> translation & transcription of new ion channels & more Na+-K+-ATP pumps
Na+-K+-ATP pumps

remove K+ from blood, forcing K+ secretion in distal tubule lumen
reabsorb Na+ from distal tubule lumen, goes into interstitial fluid, then blood
H2O follows, -> higher blood pressure

Decreased blood pressure increases renin secretion from kidney via several paths

Renin converts plasma protein to angiotensin II (ANG II) which has multiple effects to raise blood pressure and volume and maintain osmolarity

Vasoconstriction
Increases cardiovascular response
Increases vasopressin
Increases thirst
Increases aldosterone secretion, -> increases Na+ reabsorption

IV – Potassium Balance - aldosterone -> K+ excretion

Critically important as [K+] helps determine nerve and muscle membrane potential.
Low [K+] (hypokalemia) -> hyperpolarization -> muscle weakness
High [K+] (hyperkalemia) -> more excitable -> unable to repolarize fully -> less excitable -> muscle irregularities

V – Behavioral Mechanisms in Salt & Water Balance

Hypothalamic osmoreceptors detect increased osmolarity -> thirst -> drink water   -> restores volume & osmolarity
Low Na+ stimulates salt appetite
People seek shade, don’t work when it is too hot to avoid dehydration

VI – Integrated Control of Volume & Osmolarity

Kidneys, cardiovascular system, hypothalamus (thirst, vasopressin), adrenal cortex (aldosterone), more coordinate to maintain blood volume, pressure and osmolarity

Osmolarity and volume can change independently

Fig 20-17 shows 9 variations
Hemorrhage – decrease in volume, no change in osmolarity
Diarrhea or excessive sweat loss – increase in osmolarity & decrease in volume

Dehydration = decreased blood volume/pressure & increased osmolarity

Carotid & aortic baroreceptors -> raise blood pressure

Increase heart rate
Increase force of ventricular contraction
Arteriolar vasoconstriction
Decreased GFR
Increase renin secretion

Decreased blood pressure decreases GFR
Increased renin release
Stimulation of vasopressin release
Stimulation of thirst center of hypothalamus

Redundancy ensures all 4 main compensatory mechanisms are activated:

cardiovascular responses
ANG II
Vasopressin
Thirst

Results:

Restoration of volume by H2O conservation & fluid intake
Maintenance of blood pressure through increased blood volume, Increased cardiac output & vasoconstriction
Restoration of normal osmolarity by decreased Na+ reabsorption & increased H2O reabsorption & intake

VII – Acid-Base Balance

Normal body pH = 7.38-7.42
Important for tertiary structure of enzymes, membrane channels
Acidosis (low pH) -> neurons less excitable -> CNS depression (confusion, disorientation, coma)
Alkalosis (high pH) -> neurons hyperexcitable -> numbness, tingling, muscle twitches
Disturbances of acid-base balance associated with disturbances in K+ balance

Sources

Acids – CO2 most important, foods
Bases – few significant sources

pH homeostasis depends on:

buffers
ventilation
renal regulation of H+ and HCO3-

Buffers

HCO3-  most important extracellular buffer system of the body

Formed by RBCs converting CO2 -> H+ + HCO3-
Hb forms complex with H+ in RBC
HCO3- released into plasma in exchange for a Cl-

Cellular proteins and phosphate ions (HPO4 2-) also bind H+ and act as buffers in body

Increased plasma H+ (decreased pH) & plasma CO2 sensed in medulla -> increased ventilation -> decreased CO2 -> increased pH

Kidneys react to acidosis by:

combining H+  with HPO4 2- and excreting them
combining H+ with amino acids -> NH4+ and excreting them
HCO3- byproduct (H20 + CO2 -> H2CO3) reabsorbed by blood, -> more buffering capacity in proximal tubule
excreting H+ into collecting duct
collecting duct will excrete HCO3- in exchange for Cl- into interstitial space (then goes into blood)

Acid-base problems can be caused by respiratory or metabolic problems

Respiratory acidosis

Caused by alveolar hypoventilation (increased CO2)
COPD is most common cause
Renal compensation

Metabolic acidosis

Caused by excessive HCO3- loss (usually via diarrhea) or ingestion of certain fats or amino acids or anaerobic metabolism
Usually -> hyperventilation
Renal compensation also

Respiratory alkalosis

Caused by hyperventilation, usually via artificial ventilation
Renal compensation

Metabolic alkalosis

Caused by excessive vomiting of acidic stomach contents and/or excessive ingestion of bicarbonate-containing antacids
Respiratory compensation – depressed ventilation -> more CO2 retention
Renal compensation