Chapter 28: Urine Concentration and
Dilution; Regulation of ECF Osmolarity and
Sodium Concentration
Guyton and Hall, Textbook of Medical Physiology, 12th edition
Kidneys Excrete Excess Water by Forming Dilute Urine
• ADH (Vasopressin) Controls Urine Concentration
• Renal Mechanisms for Excreting Dilute Urine
Fig. 28.1 Water diuresis in a human after ingestion of 1 liter of water
Kidneys Excrete Excess Water by Forming Dilute Urine
Fig. 28.2 Formation of dilute urine when ADH levels are very low
Kidneys Excrete Excess Water (cont.)
a. Tubular fluid remains isosmotic in the proximal
tubule
b. Tubular fluid is diluted in the ascending loop of Henle
c. Tubular fluid in the distal and collecting tubules is
further diluted in the absence of ADH
Kidneys Conserve Water by Excreting Concentrated Urine
•
Water Deficit—kidney excretes solutes but reabsorbs
water therefore decreasing the volume formed
•
Urine Specific Gravity
Fig. 28.3 Relationship between specific gravity
and osmolarity of the urine
Kidneys Conserve Water by Excreting Concentrated Urine
•
Requirements for Excreting a Concentrated Urine
a. High levels of ADH
b. High osmolarity of the renal medullary interstitial
fluid
Kidneys Conserve Water by Excreting Concentrated Urine
•
Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium
a. Buildup of solute concentration in the medulla
1. Active transport of Na and cotransport
of K, Cl, and other ions from the loop of Henle
2. Active transport of ions from the collecting
ducts
3. Facilitated diffusion of urea from collecting ducts
4. Diffusion of water from the tubules
Table 28.1 Summary of tubule characteristics—urine concentration
Active NaCl
Transport
Water
Permeability
NaCl
Permeability
Urea
Permeability
Prox. Tubule
++
++
+
+
Thin
descending
0
++
+
+
Thin
Ascending
0
0
+
+
Thick
Ascending
++
0
0
0
Dist. Tubule
+
+ADH
0
0
Cortical
Coll. Tubule
+
+ADH
0
0
Inner med.
Coll. Duct
+
+ADH
0
++ADH
Conserving Water (cont.)
• Steps Involved in Causing Hyperosmotic Renal
Medullary Interstitium
Fig. 28.4 Countercurrent multiplier system in the loop of Henle for producing
a hyperosmotic renal medulla (values are in milliosmoles per liter
Conserving Water (cont.)
• Role of Distal Tubule and Collecting Ducts in
Excreting Concentrated Urine
Fig. 28.5 Formation of a concentrated urine when ADH levels are high.
Conserving Water (cont.)
• Urea Contributes to Hyperosmotic Renal Medullary
Interstitium and Formation of Concentrated Urine
• Recirculation of Urea from Collecting Duct to Loop of
Henle Contributes to Hyperosmotic Renal Medulla
a. In general the rate of urea excretion is determined by
1. The concentration of urea in the plasma
2. The glomerular filtration rate
Fig. 28.6 Recirculation of urea absorbed from the medullary collecting duct
into the interstitial fluid
Conserving Water (cont.)
• Countercurrent Exchange in the Vasa Recta
Preserves Hyperosmolarity of the Renal Medulla
a. Two features that contribute to the preservation of
high solute concentrations
1. The medullary blood flow is low
2. The vasa recta serve as countercurrent exchangers
•
Increased Medullary Blood Flow reduces Urine
Concentrating Ability
Fig. 28.7 Countercurrent exchange in the vasa recta
Conserving Water (cont.)
• Summary of Urine concentrating Mechanism and
Changes in Osmolarity in Different Segments
of the Tubules
Fig. 28.8
Control of ECF Osmolarity and Sodium Concentration
• Estimating Plasma Osmolarity from Plasma
Sodium Concentration
a. Na ions in the ECF and associated anions are
the principal determinants of fluid movement
across the cell membrane
Osmoreceptor-ADH Feedback System
Fig. 28.9 Osmoreceptor-ADH feedback
mechanism for regulating ECF
osmolarity in response to a
water deficit
Osmoreceptor-ADH Feedback System
• ADH Synthesis in the Hypothalamus and Release
from the Posterior Pituitary
Fig. 28.10
Osmoreceptor-ADH Feedback System
• Stimulation of ADH Release
a. Arterial baroreceptor reflexes
b. Cardiopulmonary reflexes
c. Decreased arterial pressure
d. Decreased blood volume
Osmoreceptor-ADH Feedback System
• Either a decrease in effective blood volume or an
increase in ECF osmolarity stimulates ADH secretion
Fig. 28.11 The effect of increased plasma
osmolarity or decreased blood
volume on the level of plasma
ADH
Importance of Thirst in Controlling ECF
Osmolarity and Na Concentration
Table 28.2 Regulation of ADH Secretion
Increase ADH
Decrease ADH
plasma osmolarity
plasma osmolarity
blood volume
blood volume
blood pressure
blood pressure
Nausea
Nausea
Hypoxia
Hypoxia
Drugs:
Drugs:
Morphine
Alcohol
Nicotine
Clonidine (antihypertensive)
Cyclophosphamide
Haloperidol (dopamine blocker)
Thirst (cont.)
• Stimuli for Thirst
a. Increased ECF osmolarity which causes intracellular
dehydration in the thirst centers
b. Decrease in ECF volume and arterial pressure
c. Production of angiotensin II
d. Dryness of the mouth and mucous membranes
e. GI and pharyngeal stimuli
•
Threshold for Drinking – when the Na concentration
increases 2 mEq/L above normal, the thirst
mechanism is activated