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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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