Unit Five: The Body Fluids and Kidneys

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 proximaltubule

b. Tubular fluid is diluted in the ascending loop of Henle

c. Tubular fluid in the distal and collecting tubules isfurther diluted in the absence of ADH

Kidneys Conserve Water by Excreting Concentrated Urine

• Water Deficit—kidney excretes solutes but reabsorbswater 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 interstitialfluid

Kidneys Conserve Water by Excreting Concentrated Urine

• Countercurrent Mechanism Produces a Hyper-osmotic 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

Active NaCl

Transport

WaterPermeabili

ty

NaClPermeabili

ty

UreaPermeabilit

y

Prox. Tubule ++ ++ + +

Thin descending

0 ++ + +

ThinAscending

0 0 + +

ThickAscending

++ 0 0 0

Dist. Tubule

+ +ADH 0 0

Cortical Coll. Tubule

+ +ADH 0 0

Inner med.Coll. Duct

+ +ADH 0 ++ADH

Table 28.1 Summary of tubule characteristics—urine concentration

Conserving Water (cont.)

• Steps Involved in Causing Hyperosmotic RenalMedullary 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 MedullaryInterstitium and Formation of Concentrated Urine

• Recirculation of Urea from Collecting Duct to Loop ofHenle Contributes to Hyperosmotic Renal Medulla

a. In general the rate of urea excretion is determined by

1. The concentration of urea in the plasma2. 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 low2. 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 andChanges in Osmolarity in Different Segmentsof the Tubules

Fig. 28.8

Control of ECF Osmolarity and Sodium Concentration

• Estimating Plasma Osmolarity from PlasmaSodium Concentration

a. Na ions in the ECF and associated anions arethe principal determinants of fluid movementacross 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 Releasefrom 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 anincrease 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

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)

Table 28.2 Regulation of ADH Secretion

Thirst (cont.)

• Stimuli for Thirst

a. Increased ECF osmolarity which causes intracellulardehydration in the thirst centers

b. Decrease in ECF volume and arterial pressurec. Production of angiotensin IId. Dryness of the mouth and mucous membranese. GI and pharyngeal stimuli

• Threshold for Drinking – when the Na concentrationincreases 2 mEq/L above normal, the thirst mechanism is activated