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Osmoregulation (Water Balance)

- involves regulation of body fluid osmolarity (concentration) and total fluid volume


To maintain steady state

water gain = water loss
urine is a major avenue of water loss (~ 1.5 L/day)
kidneys conserve water, control volume and concentration of urine excreted


. Regulation of ECF Osmolarity

- ECF osmolarity affects H2O movement in and out of cells
normal ECF osmolarity = 290 mOsm
↑ ECF osmolarity → ↓ ICF volume
↓ ECF osmolarity → ↑ ICF volume



osmoreceptors respond to high plasma osmolarity
neurosecretory cells produce ADH (vasopressin), secreted by posterior pituitary


high ADH levels

↑ permeability of CD to H2O
→ ↑ H2O reabsorbed from CD
→ concentrated urine, less H2O lost


low ADH levels

↓ permeability of CD to H2O
→ ↓ H2O reabsorbed from CD
→ dilute urine, more H2O lost
(e.g. diabetes insipidus)


Negative feedback control

↑ ECF osmolarity → ↑ ADH secretion → ↑ H2O reabsorption from CD → ↓ ECF osmolarity


Regulation of ECF Volume

- ECF volume affects blood pressure
- kidneys help control ECF volume
- Na+ and Cl
- are the most abundant ECF solutes
- total amount of Na+ in the ECF affects ECF volume
↑ Na+ in ECF → ↑ ECF osmolarity → ↑ ADH → ↑ H2O reabsorption → ↑ ECF volume


kidneys help control ECF volume via:

1. regulation of H2O reabsorption/ excretion - controlled by ADH
2. regulation of solute reabsorption/ excretion


Fluid imbalances may involve change in

osmolarity, volume, or both.
e.g., hypertonic dehydration: ↑ ECF osmolarity and ↓ ECF volume
isotonic dehydration: ↓ ECF volume with normal ECF osmolarity


. Electrolyte Balance: Na+ and K+ Regulation

- most Na+ and K+ filtered into nephrons is reabsorbed in the PCT
- regulated reabsorption and secretion of Na+ and K+ in the DCT and upper CD



secreted by the adrenal cortex
- stimulates Na+ reabsorption and K+ secretion in principle (P) cells of DCT and CD
- activates apical Na+ and K+ channels and basolateral Na+-K+ pumps


What does ICF volume depend on?
what decreases ICF volume?

ECF osmolarity

Increase in ECF concentration decreases ICF volume


aldosterone secretion is stimulated by

1. high plasma [K+]
2. renin-angiotensin-aldosterone system


renin-angiotensin-aldosterone system

responds to low BP and low [Na+]
juxtaglomerular apparatus
angiotensin II effects


juxtaglomerular apparatus

granular (juxtaglomerular) cells - sense BP in afferent arteriole
macula densa - senses [Na+] in tubular fluid


in blood
in capillaries

- enzyme secreted into blood by granular cells
in blood, renin converts angiotensinogen to angiotensin I
in capillaries, angiotensin converting enzyme (ACE) converts ANG I to ANG II


angiotensin II effects

1. vasoconstriction →  peripheral resistance →  BP
2. stimulates aldosterone secretion →  Na+ reabsorption →  plasma volume →  BP


Renal Acid-Base Regulation

Kidneys control excretion of metabolic (non-CO2) acids and bases
- normally secrete H+ and reabsorb HCO3-
- rates of H+ secretion and HCO3-
- reabsorption are adjusted to respond to alterations in
pH and [HCO3-] of the plasma
- net result is regulation of plasma [HCO3-] and pH


Negative feedback control
Normal pH and [HCO3-]

normal pH = 7.4 and [HCO3-] = 24 mM
decrease [HCO3-] and/or in pH -> increase in H+ secretion and increase in HCO3- reabsorption → increase [HCO3-], increase pH

increase [HCO3-] and/or in pH → decrease in H+ secretion and HCO3- reabsorption → decrease [HCO3-], decrease in pH


Mechanism of bicarbonate reabsorption

1. HCO3
- in tubular fluid (PCT and DCT) combines with H+ to form CO2 + H2O
(catalyzed by carbonic anhydrase in the tubule)
2. CO2 diffuses into the tubule epithelial cells
3. CO2 is converted to H+ + HCO3
- (via carbonic anhydrase inside the cell)
4. HCO3
- is transported to ECF,
H+ is pumped back out to the tubule lumen