Tubular Reabsorption Figure 27-1; Guyton and Hall

Primary Active Transport of Na+ Figure 27-2; Guyton and Hall

Mechanisms of Secondary Active Transport Figure 27-3; Guyton and Hall

Glucose Transport Maximum Figure 27-4; Guyton and Hall

Reasorption of Water and Solutes is Coupled to Na+ Reabsorption Interstitial Fluid Tubular Cells Tubular Lumen - 70 mV Na + H + Na + glucose, amino acids Na + ATP K+ Urea Na + H20 ATP Na + K+ Cl- 0 mv - 3 mV Copyright © 2006 by Elsevier, Inc.

Mechanisms by which Water, Chloride, and Urea Reabsorption are Coupled with Sodium Reabsorption Figure 27-5; Guyton and Hall

Cellular Ultrastructure and Primary Transport Characteristics of Proximal Tubule Figure 27-6; Guyton and Hall

Cellular Ultrastructure and Transport Characteristics of Thin and Thick Loop of Henle very permeable to H2O) not permeable to H2O) Figure 27-8; Guyton and Hall

Sodium Chloride and Potassium Transport in Thick Ascending Loop of Henle Figure 27-9; Guyton and Hall

Countercurrent Multiplier System in the Loop of Henle Figure 28-3; Guyton and Hall

Countercurrent multiplier animation

Recirculation of Urea Absorbed from Medullary Collecting Duct into Interstitial Fluid Figure 28-5; Guyton and Hall

Net Effects of Countercurrent Multiplier 1. More solute than water is added to the renal medulla (i.e., solutes are “trapped” in the renal medulla). 2. Fluid in the ascending loop is diluted. 3. Horizontal gradient of solute concentration established by the active pumping of NaCl is “multiplied” by countercurrent flow of fluid.

The Vasa Recta Preserve Hyperosmolarity of Renal Medulla serve as countercurrent exchangers Vasa recta blood flow is low (only 1-2 % of total renal blood flow) Figure 28-3; Guyton and Hall

Sodium Chloride Transport in Early Distal Tubule Figure 27-10; Guyton and Hall

Cellular Ultrastructure and Transport Characteristics of Early and Late Distal Tubules and Collecting Tubules not permeable to H2O not very permeable to urea permeability to H2O depends on ADH not very permeable to urea Figure 27-11; Guyton and Hall

Sodium Chloride Reabsorption and Potassium Secretion in Collecting Tubule Principal Cells Figure 27-12; Guyton and Hall

Cortical Collecting Tubules Intercalated Cells Tubular Cells Tubular Lumen H20 (depends on ADH) H + K+ ATP ATP K+ Na + H+ ATP ATP K+ ATP Cl - Copyright © 2006 by Elsevier, Inc.

Cellular Ultrastructure and Transport Characteristics of Medullary Collecting Tubules Figure 27-13; Guyton and Hall

Normal Renal Tubular Na+ Reabsorption (1789 mEq/d) 7 % (16,614 mEq/day) 65 % 25,560 mEq/d 25 % (6390 mEq/d) 2.4% (617 mEq/day) 0.6 % (150 mEq/day) Copyright © 2006 by Elsevier, Inc.

Summary of Water Reabsorption and Osmolarity in Different Parts of the Tubule Proximal Tubule: 65% reabsorption, isosmotic Desc. loop: 15-20% reabsorption, osmolarity increases Asc. loop: 0% reabsorption, osmolarity decreases Early distal: 0% reabsorption, osmolarity decreases Late distal and coll. tubules: ADH dependent water reabsorption and tubular osmolarity Medullary coll. ducts: ADH dependent water reabsorption and tubular osmolarity

Minimal urine concentration Concentration and Dilution of the Urine Maximal urine concentration = 1200 - 1400 mOsm / L (specific gravity ~ 1.030) Minimal urine concentration = 50 - 70 mOsm / L (specific gravity ~ 1.003)

Obligatory Urine Volume The minimum urine volume in which the excreted solute can be dissolved and excreted. Example: If the max. urine osmolarity is 1200 mOsm/L, and 600 mOsm of solute must be excreted each day to maintain electrolyte balance, the obligatory urine volume is: 600 mOsm/d 1200 mOsm/L = 0.5 L/day

Maximum Urine Concentration of Different Animals Animal Max. Urine Conc. (mOsm /L) Beaver 500 Pig 1,100 Human 1,400 Dog 2,400 White Rat 3,000 Kangaroo Mouse 6,000 Australian Hopping Mouse 10,000

H20 (w/o ADH) Aldosterone Late Distal, Cortical and Medullary Collecting Tubules Principal Cells Tubular Lumen H20 (w/o ADH) Na + Na + ATP ATP K+ K+ Cl - Aldosterone Copyright © 2006 by Elsevier, Inc.

Abnormal Aldosterone Production Excess aldosterone - Conn’s syndrome Na+ retention, hypokalemia, alkalosis, hypertension Aldosterone deficiency - Addison’s disease Na+ wasting, hyperkalemia, hypotension, death if untreated

Ang II Increases Tubular Na+ Transport Cells Interstitial Fluid Tubular Lumen Ang II Ang II + Na+ Na ATP K + H+ Copyright © 2006 by Elsevier, Inc.

Ra Re Effect of Angiotensin II on Peritubular Capillary Dynamics Glomerular Capillary Peritubular Capillary Ra Re Arterial Pressure Re Pc (peritubular cap. press.) Ang II renal blood flow FF c

Ang II Constriction of Efferent Arterioles Causes Na+ Retention and Maintains Excretion of Waste Products Na+ depletion Ang II Resistance efferent arterioles Glom. cap. press Renal blood flow Peritub. Cap. Press. Prevents decrease in GFR and retention of waste products Filt. Fraction Na+ and H2O Reabs. Copyright © 2006 by Elsevier, Inc.

Angiotensin II Blockade Decreases Na+ Reabsorption and Blood Pressure ACE inhibitors (captopril, benazipril, ramipril) Ang II antagonists (losartan, candesartin, irbesartan) decrease aldosterone directly inhibit Na+ reabsorption decrease efferent arteriolar resistance Natriuresis and Diuresis + Blood Pressure

Formation of a Dilute Urine Continue electrolyte reabsorption Decrease water reabsorption Mechanism: decreased ADH release and reduced water permeability in distal and collecting tubules Figure 28-1; Guyton and Hall

Formation of a Concentrated Urine Continue electrolyte reabsorption Increase water reabsorption Mechanism: Increased ADH release which increases water permeability in distal and collecting tubules High osmolarity of renal medulla Countercurrent flow of tubular fluid

Formation of a Concentrated Urine when Antidiuretic Hormone (ADH) Levels are High Figure 28-4; Guyton and Hall

Osmoreceptor– antidiuretic hormone (ADH) feedback mechanism for regulating extracellular fluid osmolarity Figure 28-8; Guyton and Hall

ADH synthesis in the neurons of hypothalamus, release by the posterior pituitary, and action on the kidneys Figure 28-9; Guyton and Hall

Factors that Decrease ADH Secretion Decreased osmolarity Increased blood volume (cardiopulmonary reflexes) Increased blood pressure (arterial baroreceptors) Other factors: - alcohol - haloperidol (antipsychotic, tics,Tourette’s)

Stimuli for Thirst Increased osmolarity Decreased blood volume (cardiopulmonary reflexes) Decreased blood pressure (arterial baroreceptors) Increased angiotensin II Other stimuli: - dryness of mouth

Factors that Decrease Thirst Decreased osmolarity Increased blood volume (cardiopulmonary reflexes) Increased blood pressure (arterial baroreceptors) Decreased angiotensin II Other stimuli: -Gastric distention

Atrial Natriuretic Peptide (ANP) Blood volume ANP Renin release aldosterone GFR Ang II Renal Na+ and H2O reabsorption Na+ and H2O excretion

Late Distal and Collecting Tubules Tubular Cells Tubular Lumen H20 (depends on ADH) H20 Aquaporin-2 Aquaporin-3 Aquaporins ADH cAMP Vesicle V2 receptor Copyright © 2006 by Elsevier, Inc.

Sodium Chloride and Potassium Transport in Thick Ascending Loop of Henle Figure 27-9; Guyton and Hall

Sodium Chloride Transport in Early Distal Tubule Figure 27-10; Guyton and Hall

Sodium Chloride Reabsorption and Potassium Secretion in Collecting Tubule Principal Cells Figure 27-12; Guyton and Hall