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Figure 1-1  A cross-section of the renal architecture
Figure 1-2  Major sections of the nephrons and their position within the cortex and medulla.
Figure 1-3  A cartoon of the nephron and its associated blood supply. The basic steps in urine formation are illustrated. 1. Filtration. 2. Reabsorption. 3. Secretion. 4. Excretion.

Figure 2-1  Pressure gradients and control points in the renal circulation. H.P. = hydrostatic pressure. pb = colloid osmotic pressure.
Figure 2-2  Balance between hydrostatic and colloid osmotic pressures in the two capillary beds.
Figure 2-3 The filtration pathway.
Figure 2-4  Pressures involved in filtration.
Figure 2-5  Hydrostatic and colloid osmotic pressure profiles in the glomerular capillary bed.
Figure 2-6  Effect of factors altering pressures in the glomerular capillaries on mean filtration rate.
Figure 2-7  Effect of changes in afferent and arteriolar resistance on GFR and RBF.
Figure 2-8  The juxtaglomerular apparatus.
Figure 2-9  The juxtaglomerular apparatus is a major control point.
Figure 2-10  Autoregulation. The effect of changes in arterial pressure on RBF and GFR.
Figure 2-11  The tubuloglomerular feedback mechanism.
Figure 2-12  The effect of the autoregulatory mechanisms and PGE2 on the response of the renal arterioles to extrinsic factors.

Figure 3-1  The basic structure of epithelial cell layers.  The width of the zonula occludens and the paracellular space have been greatly exaggerated for purposes of emphasis.
Figure 3-2  Changes in the urine to plasma concentration ratio (Ux/Px) of various substances along the length of the nephron.  Note that the ordinate is a log scale.
Figure 3-3. Changes in the fraction of the filtered amount of substances remaining in the tubular fluid along the length of the nephron.
Figure 3-4. An example of the generation of a transepithelial electrical gradient by a tubular cell. 
Figure 3-5. An illustration of a gradient-limited transport system.

Figure 4-1. Measurement of filtration rate. 
Figure 4-2.
Measurement of solute reabsorption rate.
Figure 4-3. Measurement of solute secretion rate.
Figure 4-4. Effect of plasma concentration of a substance on its clearance. A. Substance that is filtered only. B. Substance that is reabsorbed. C. Substance that is secreted.
Figure 4-5. The effect of changes in Pg on its rates of filtration, reabsorption, excretion and clearance.
Figure 4-6. Changes in plasma creatinine concentration and 1/Pcr as a function of changes in GFR.
Figure 4-7. Illustration of the utility of measuring Pcr in a patient with chronic renal disease.
Figure 4-8. Calculation of fractional water excretion.
Figure 4-9. Calculation of the fractional excretion of a solute, FEs.

Figure 5-1. The effect changes in urine flow rate on the fractional excretion of urea.
Figure 5-2. Proximal tubule reabsorption and secretion of urate.
Figure 5-3. Transport mechanisms for glucose reabsorption in the proximal tubule.

Figure 6-1. The transepithelial chemical and electrical gradients along the length of the proximal tubule. TF/P = tubular fluid to plasma concentration ratio; Vt = transepithelial voltage gradient; A.A. = amino acids.
Figure 6-2. The mechanisms for Na reabsorption in the proximal tubule.
Figure 6-3. The mechanism for HCO3 reabsorption in the proximal tubule.
Figure 6-4. Mechanisms for Cl reabsorption in the proximal tubule.
Figure 6-5. Water reabsorption in the proximal tubule.
Figure 6-6. Mechanisms for NaCl reabsorption in the thick ascending limb of the loop of Henle.
Figure 6-7. Mechanisms of NaCl reabsorption in the distal convoluted tubule.
Figure 6-8. Na+ and Cl- reabsorption by the principal cells in the collecting tubule.

Figure 7-1. The negative feedback mechanism that regulates the osmotic concentration of the extracellular fluid.
Figure 7-2. The relationship between the plasma osmotic concentration and plasma ADH concentration. The maximum effective concentration is that which causes the kidney to maximally concentrate the urine.
Figure 7-3. The mechanism of action of ADH on principal cells. V2 = vasopressin 2 receptor. Gs = stimulatory G protein, AC = adenylyl cyclase, AQ2 = aquaporin 2.
Figure 7-4. An illustration of the use of the countercurrent principle to conserve heat and improve the efficiency of a furnace. The thick arrows indicate the direction of heat flow.
Figure 7-5. The loop of Henle, the "countercurrent multiplier". The numbers indicate the osmotic concentration. The large circles to the right represent cross-sections of the medulla. Dlh, alh = descending and ascending limbs of Henle's loop.
Figure 7-6. The role of the distal tubule and collecting tubule in the countercurrent process. CD = collecting tubule.
Figure 7-7. The vasa recta, the "countercurrent exchanger". Dvr, avr = descending and ascending vasa recta.
Figure 7-8. Countercurrent concentration of urea by the vasa recta and inner medullary collecting tubules.
Figure 7-9. An illustration of the effect of an increase to flow on net Na reabsorption.

Figure 8-1. The vascular compartment, its subdivisions, its relation to the interstitial compartment and the location of receptors.
Figure 8-2.
Role of the atria as volume receptors.
Figure 8-3. The signals that impinge upon the juxtaglomerular apparatus in response to vascular volume changes and the effector mechanisms controlled by the apparatus.
Figure 8-4. The relative effects of osmolality, blood volume and arterial pressure on plasma ADH concentration.
Figure 8-5. Role of ANF in response to changes in blood volume.
Figure 8-6. The effect of changes in GFR on reabsorption and excretion of salt and water. FR = fractional reabsorption. FE = fractional excretion
Figure 8-7. The effect of blood volume expansion on pressures in the peritubular capillaries.
Figure 8-8. The three factors that act upon the j.g. apparatus to increase the secretion of renin.
Figure 8-9. The role of efferent sympathetic nerve activity (ESNA) in the response to volume changes.
Figure 8-10. The various factors that respond to severe volume depletion and act to reduce the excretion of salt and water.
Figure 8-11. The various factors that respond to acute volume expansion and act to increase salt and water excretion.

Figure 9-1. The acid-base buffering systems of the body. The arrows across the box representing the kidney indicate excretion only. They are not meant to convey any information on the renal mechanism involved.
Figure 9-2A. Na-H exchanger and Na-HCO3 cotransporter in proximal tubule.
Figure 9-2B. Proton ATPase, Cl-HCO3 exchanger and Cl channel in intercalated cells.
Figure 9-2C.  H-K exchanger in intercalated cells.
Figure 9-3. The factors controlling the rate of proton secretion.
Figure 9-4. The reactions of tubular fluid buffers with secreted protons.
Figure 9-5. The factors controlling the rates of HCO3 reabsorption and excretion.
Figure 9-6. The quantitative relationship between the plasma HCO3 concentration and the rates of filtration, reabsorption and excretion.
Figure 9-7. The factors regulating the rates of acid titration and excretion.
Figure 9-8. The balance between proton secretion and HCO3 filtration determines the renal reaction to acid-base disturbances.
Figure 9-9. Changes in blood composition during hypoventilation.
Figure 9-10. Changes in blood composition during metabolic alkalosis.
Figure 9-11. Metabolic reactions involved in renal production of ammonia. PDG = phosphate dependent glutaminase. GDH = glutamate dehydrogenase. NAD = nicotinamide adenine dinucleotide.

Figure 10-1. Schematic representation of total body potassium distribution and the maintenance of potassium homeostasis.
Figure 10-2. Tubular sites of K transport. The numbers indicate the average amount of K that reaches each segment per day. The curve shows the changes in tubular fluid K concentration, relative to plasma concentration, as both K and H2O are transported.
Figure 10-3. The mechanisms of K secretion in the late distal tubule and in the collecting tubule.
Figure 10-4. Factors that stimulate K secretion.
Figure 10-5. Effects on K secretion of changes in flow rate, tubular fluid [Na], and [Cl]. Shaded areas show approximate physiological range.

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