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THIRD EDITION

HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
Dee Unglaub Silverthorn, Ph.D.

Chapter 20, part B


Integrative Physiology II:
Fluid and Electrolyte Balance
PowerPoint Lecture Slide Presentation by
Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Sodium Recycling: Recycling and Excretion


Ascending loop of Henle
H2O impermeable
Na+ Active Transport
To ECF
Gradient
Diffuses to blood
Collecting Duct:
Aldosterone regulates
Na+ recycled or excreted
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Mechanism of Na+ Selective Reabsorption in


Collecting Duct

Aldosterone: steroid H from adrenal cortex


Stimulates Na+ uptake (& K+ secretion)
channel synthesis

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Mechanism of Na+ Selective Reabsorption in


Collecting Duct

Figure 20-12: Aldosterone action in principal cells


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Angiotensin Pathway: Maintains BP , Volume &


Osmolarity Angiotensinogen, ANGI, ANG II, rennin,
& ACE

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Figure 20-13: The renin-angiotensin-aldosterone pathway

Artial Natruretic Peptide: Regulates Na+ & H2O


Excretion

Hormone from myocardial cells


Stimulates: hypothalamus, kidney, adrenal, &
medulla

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Artial Naturetic Peptide: Regulates Na+ & H2O


Excretion

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-15: Atrial natriuretic peptide

Potassium Balance:
Critical for Excitable Heart & Nervous Tissues

Hypokalemia low [K+] in ECF, Hyperkalemia high [K+]


Reabsorbed in Ascending Loop, secreted in
Collecting duct

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Potassium Balance:
Critical for Excitable Heart & Nervous Tissues

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-4: Osmolarity changes as fluid flows through the nephron

Potassium Balance:
Critical for Excitable Heart & Nervous Tissues

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-12: Aldosterone action in principal cells

Response to Dehydration & Osmolarity Imbalance

Thirst & "salt craving", or avoidance behavior


Integrated circulatory & excretory reflexes

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Response to Dehydration & Osmolarity Imbalance

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-17 : Homeostatic compensation for severe dehydration

Acid/Base Homeostasis: Overview


Acidosis: plasma pH
Protein damage
CNS depression
Alkalosis: plasma pH
Hyperexcitability
CNS & heart
Buffers: HCO3- & proteins
H+ input: diet & metabolic
H+ output: lungs & kidney
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Acid/Base Homeostasis: Overview

Figure 20-18: Hydrogen balance in the body


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Kidney Hydrogen Ion Balancing: Proximal Tubule

H+ & NH4+ secreted into lumen and excreted


HCO3- is reabsorbed

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Kidney Hydrogen Ion Balancing: Proximal Tubule

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-21: Proximal tubule secretion and reabsorption of filtered HCO 3-

Kidney Hydrogen Ion Balancing: Collecting Duct

Type A Intercalated cells excrete H+ absorb HCO3 Type B intercalated cells absorb H+ secrete HCO3-

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Kidney Hydrogen Ion Balancing: Collecting Duct

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 20-22: Role of the intercalated cell in acidosis and alkalosis

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Classifications of Acute Kidney Injury and Chronic Kidney Disease.

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Pathophysiological Features of Acute Kidney Injury Leading to


Chronic Kidney Disease.

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 1
An overview of the pathogenesis of CKD
progression. Although there is considerable
interaction between BP-dependent and BPindependent initiating mechanisms, BPdependent mechanisms predominate in
hypertensive CKD states. BP independent
mechanisms may modulate hypertensive injury
and also contribute to CKD progression in
normotensive states. AR, autoregulation; BP,
blood pressure; CKD, chronic kidney disease; NO,
nitric oxide; RAAS, reninangiotensin
aldosterone system; ROS, reactive oxygen species
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Summary
Electrolyte balance depends on integration of
circulatory, excretory and behavioral physiology
Water recycling and ECF/plasma balance
depends on descending loop of Henle and
vasopressin regulated collecting duct for
conservation
Osmolarity depends on aldosterone and
angiotensin pathway to regulate CNS & endocrine
responses
Along with respiration, proximal tubule and
collecting duct cells reabsorb or excrete H+ &
HCO3- to balance pH
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

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