Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Dee Unglaub Silverthorn, Ph.D. H UMAN P HYSIOLOGY PowerPoint ® Lecture Slide Presentation by Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University AN INTEGRATED APPROACH T H I R D E D I T I O N Chapter 20, part B Integrative Physiology II: Fluid and Electrolyte Balance

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Sodium Recycling: Recycling and Excretion Ascending loop of Henle H 2 O impermeable Na + Active Transport To ECF Gradient Diffuses to blood Collecting Duct: Aldosterone regulates Na + recycled or excreted

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Aldosterone: steroid H from adrenal cortex Stimulates Na + uptake (& K + secretion)  channel synthesis Mechanism of Na + Selective Reabsorption in Collecting Duct

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Mechanism of Na + Selective Reabsorption in Collecting Duct Figure 20-12: Aldosterone action in principal cells

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 20-13: The renin-angiotensin-aldosterone pathway Angiotensin Pathway: Maintains BP, Volume & Osmolarity Angiotensinogen, ANGI, ANG II, rennin, & ACE

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings 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 + & H 2 O Excretion Figure 20-15: Atrial natriuretic peptide

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings 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 Figure 20-4: Osmolarity changes as fluid flows through the nephron

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Potassium Balance: Critical for Excitable Heart & Nervous Tissues Figure 20-12: Aldosterone action in principal cells

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Thirst & "salt craving", or avoidance behavior Integrated circulatory & excretory reflexes Response to Dehydration & Osmolarity Imbalance

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Response to Dehydration & Osmolarity Imbalance Figure : Homeostatic compensation for severe dehydration

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Acidosis:  plasma pH Protein damage CNS depression Alkalosis:  plasma pH Hyperexcitability CNS & heart Buffers: HCO 3 - & proteins H + input: diet & metabolic H + output: lungs & kidney Acid/Base Homeostasis: Overview

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Acid/Base Homeostasis: Overview Figure 20-18: Hydrogen balance in the body

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings H + & NH 4 + secreted into lumen and excreted HCO 3 - is reabsorbed Kidney Hydrogen Ion Balancing: Proximal Tubule

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Kidney Hydrogen Ion Balancing: Proximal Tubule Figure 20-21: Proximal tubule secretion and reabsorption of filtered HCO 3 -

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Type A Intercalated cells excrete H + absorb HCO 3 - Type B intercalated cells absorb H + secrete HCO 3 - Kidney Hydrogen Ion Balancing: Collecting Duct

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Kidney Hydrogen Ion Balancing: Collecting Duct Figure 20-22: Role of the intercalated cell in acidosis and alkalosis

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

Classifications of Acute Kidney Injury and Chronic Kidney Disease.

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Pathophysiological Features of Acute Kidney Injury Leading to Chronic Kidney Disease.

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 BPdependent and BP- independent initiating mechanisms, BP- dependent 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, renin–angiotensin– 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 + & HCO 3 - to balance pH