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Tubular fluid
Filtrate after it leaves Bowman’s capsule
Tubular flow order
PCT → Loop of Henle → DCT → Collecting tubule → Collecting duct
Tubular reabsorption
Movement of substances from tubular fluid back to blood
Tubular secretion
Movement of substances from blood into tubular fluid
Excretion equation
Excretion = Filtration − Reabsorption + Secretion
How much glucose is reabsorbed?
~100% reabsorbed
Bicarbonate reabsorption
99.9% reabsorbed
Sodium reabsorption
~99.4% reabsorbed
Chloride reabsorption
~99.1% reabsorbed
Potassium reabsorption
~87.8% reabsorbed
Urea reabsorption
~50% reabsorbed
Creatinine reabsorption
0% (fully excreted)
Types of reabsorption
Active and passive
Water reabsorption mechanism
Osmosis following solute
Transcellular transport
Through cells
Paracellular transport
Between cells
Na+ transport mechanism
Active transport via Na+/K+ ATPase
Na+ importance
Drives most reabsorption
Cl- reabsorption
Passive diffusion
Urea permeability
Lower than chloride
Transport maximum (Tm)
Max rate of carrier-mediated transport
When Tm exceeded
Substance appears in urine
Proximal tubule (PCT)
Reabsorbs ~65% of filtrate
PCT reabsorbs
Na+, Cl-, HCO3-, K+, water, glucose, amino acids
PCT secretion
H+, organic acids, toxins
Glucose reabsorption mechanism
Na+ cotransport (SGLT)
Amino acid reabsorption
Na+ cotransport
Na+ countertransport
Exchanged with H+
Na+/K+ pump location
Basolateral membrane
Water reabsorption in PCT
Follows Na+ osmotically
PCT reabsorption type
Isosmotic
Hormone affecting PCT
Angiotensin II increases Na+ reabsorption
CO2 role in PCT
Helps buffer regulation via HCO3-
Passive ion reabsorption
Driven by gradients and permeability
PCT secretion examples
Bile salts, urate, drugs
Glucose threshold
Point where glucose appears in urine
Reason glucose appears before Tm
Transporters saturate unevenly
Proximal tubule concentration ratio (=1)
Same concentration as filtrate
Ratio <1
More reabsorbed than water
Ratio >1
Less reabsorbed than water
Loop of Henle
Concentrates urine via countercurrent system
Descending limb
Permeable to water
Ascending limb
Impermeable to water
Thin descending limb
Water reabsorption only
Thick ascending limb
Reabsorbs Na+, Cl-, K+
Ascending limb fluid
Hypo-osmotic
Water reabsorbed in descending limb
~50% of water
NaCl reabsorbed in ascending limb
~2/3
Countercurrent exchange
Maintains gradient
Countercurrent multiplication
Creates gradient
Distal tubule receives
~15–20% of filtrate
Distal tubule reabsorption
Variable and hormone-controlled
What type of transport is Na+ reabsorption in DCT?
Active transport
Aldosterone function
Increases Na+ reabsorption
Effect of aldosterone
Reduces Na+ loss in urine
ANP/BNP effect
Opposes aldosterone
Water reabsorption in DCT
Follows Na+
Ca2+ reabsorption
Controlled by PTH and calcitriol
K+ secretion in DCT
Exchange with Na+
Source of secreted K+
Peritubular fluid
H+ secretion in DCT
Exchange with Na+
H+ role
Regulates acid-base balance
H+ source
Carbonic acid dissociation
Aldosterone effect on H+
Increases secretion
Collecting duct
Final regulation of urine
Collecting duct receives
Fluid from multiple nephrons
Hormones controlling collecting duct
Aldosterone and ADH
ADH function
Increases water permeability
Aldosterone function
Increases Na+ pumps
Medullary collecting duct
Highly permeable to water
Medulla osmolarity
~4x greater than cortex
Na+ reabsorption in CD
Aldosterone-dependent
HCO3- reabsorption
Exchanged for Cl-
Urea reabsorption
Diffuses out of duct
H+ secretion in CD
Depends on pH
Low pH
Secrete H+
High pH
Secrete bicarbonate
Water balance goal
Maintain ECF osmolarity
Extracellular water determined by
Intake + renal excretion
Urine osmolarity range
~50 to 1400 mOsm/L
Dilute urine
Occurs with excess water
Concentrated urine
Occurs with dehydration
Water excretion independence
Independent of solute excretion
Filtrate reabsorbed before DCT
~85%
Effect of drinking water
Increased urine volume
Solute excretion
Remains relatively constant
Formation of dilute urine
NaCl reabsorption without water
Ascending limb role
Creates dilute tubular fluid
Late DCT/CD
Further dilute urine
ADH (vasopressin)
Controls water reabsorption
ADH release trigger
High ECF osmolarity
ADH target
DCT, collecting tubule, collecting duct
Aquaporins
Water channels inserted by ADH
Diuresis
Low ADH → more urine
Antidiuresis
High ADH → concentrated urine
Obligatory urine volume
Minimum urine needed to excrete solutes
Seawater example
Causes dehydration (too much solute)
Requirements for concentrated urine
High ADH + high medullary osmolarity
Medullary gradient
300 → 1200–1400 mOsm
Single effect
~200 mOsm gradient created