Integrative Physiology II: Fluid and Electrolyte Balance Chapter 20 Integrative Physiology II: Fluid and Electrolyte Balance

Figure 20-3: Role of the kidneys in water balance Body Water Balance Urine concentration: Dilute: 300 mOsM Concentrated: 1200 mOsM Figure 20-3: Role of the kidneys in water balance

What is “put back” and where in the nephron. Proximal tubule Glucose (those carriers) & Na+ (Primary active transport) urea (passive transport) Loop of Henle H2O and ions ( Na+, K+ & Cl-) Distal tubule Na+ & H2O Collecting duct H2O, Na+ & urea (again)

Overview: starts off isosmotic 300 mOsM (saltiness) Figure 20-4: Osmolarity changes as fluid flows through the nephron

VASOPRESSIN: If we NEED water, we can get it from the collecting duct!

Vasopressin (a.k.a. ADH) regulates urine OsM: Let’s make concentrated uring part I Figure 20-5: Water movement in the collecting duct in the presence and absence of vasopressin

Formation of Water Pores: Mechanism of Vasopressin Action

Figure 20-7: Factors affecting vasopressin release

Figure 20-10: Countercurrent exchange in the medulla of the kidney Countercurrent exchanger. Loop of Henle Let’s make concentrated uring part II Medullary osmotic gradient; more salty Collecting duct Figure 20-10: Countercurrent exchange in the medulla of the kidney

Why is it, countercurrent? The players: Loop of Henle Descending/ascending vasa recta Ions: which ones? H2O Why is it, countercurrent?

Key facts: 1. descending LOH is water permeable, ascending LOH is NOT. 2. Ascending LOH actively pumps out ions. 3. water goes to where the most stuff is!!! 4. vasa recta removes water so it doesn’t dilute the medullary gradient.

SODIUM BALANCE: What happens to the body’s OsM after eating salty fries? Increase/decrease This triggers two responses; can you guess?

Vassopressin and thirst; both decrease OsM, but raise blood pressure. To lower blood pressure our kidneys excrete sodium. How does excreting sodium lower BP?

WATER GOES TO WHERE THE MOST STUFF IS. When sodium leaves, water follows, decreasing ECF volume, and BP.

Sodium Balance: Intake & Excretion Figure 20-11: Homeostatic responses to eating salt

Sodium is regulated by aldosterone from the adrenal cortex. Aldosterone is actually secreted in response to blood pressure, blood volume and OsM. More aldosterone: more sodium reabsorption. Aldosterone target: principal cell (P cell) of the distal tubule & collecting duct.

Mechanism of Na+ Selective Reabsorption in Collecting Duct !water does not follow! Vassopressin must be present Figure 20-12: Aldosterone action in principal cells

How does aldosterone get released How does aldosterone get released? RAAS: renin-angiotensin-aldosterone-system Figure 20-13: The renin-angiotensin-aldosterone pathway

Artial Natruretic Peptide: Regulates Na+ & H2O Excretion 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

Potassium Balance: Critical for Excitable Heart & Nervous Tissues Figure 20-4: Osmolarity changes as fluid flows through the nephron

Potassium Balance: Critical for Excitable Heart & Nervous Tissues Figure 20-12: Aldosterone action in principal cells

Integrative Physiology II: acid-base balance Chapter 20, part B Integrative Physiology II: acid-base balance

Acid/Base Homeostasis Acidosis:  plasma pH Protein damage CNS depression Alkalosis:  plasma pH Hyperexcitability CNS & heart Buffers: HCO3- & proteins H+ input: diet & metabolic H+ output: lungs & kidney Neutral pH is 7.0 Biological pH is 7.4 Determined based upon H+ concentration.

Acid/Base Homeostasis: Overview Figure 20-18: Hydrogen balance in the body

Low pH – acidosis – nervous tissue becomes less exciteable – respiratory centers shut down. High pH – alkalosis – neurons become hyperexciteable – twitching, numbness – tetenay and paralyzed respiratory muscles.

pH homeostasis depends on 3 things: 1. buffers 2. the lungs 3. the kidneys

Buffer systems Bicarbonate, phosphate ions, and proteins (Hb) Buffers prevent significant changes in pH by binding or releasing H+ CO2 + H2O H2CO3 H+ + HCO3- carbonic anhydrase

What will drive the equation to the right? What will drive the equation to the left? CO2 + H2O H2CO3 H+ + HCO3- carbonic anhydrase How can ventilation compensate for pH disturbances? Pg. 647.

Acidosis prevention at the Proximal Tubule: H+ excreted, bicarbonate reabsorption. Na+ - H+ antiport activity Glutamine metabolism Figure 20-21: Proximal tubule secretion and reabsorption of filtered HCO3-

Kidney Hydrogen Ion Balancing: Collecting Duct Type A Intercalated cells excrete H+ absorb HCO3- Type B intercalated cells absorb H+ secrete HCO3-

Kidney Hydrogen Ion Balancing: Collecting Duct The polarity of the two cells is reversed with the transport proteins on opposite sides. Figure 20-22: Role of the intercalated cell in acidosis and alkalosis

Acid-base disturbances: respiratory or metabolic Respiratory acidosis – hypoventilation & CO2 retention. COPD- loss of alveolar tissue Metabolic acidosis Metabolic acids increase protons Lactic acid from anaerobic metabolism burn sugar not oxygen. Respiratory alkalosis Hyperventilation rids CO2 Hysterical hyperventilation Renal compensation can occur Metabolic alkalosis Vomiting stomach acids and taking bicarbonate-containing antacids. Respiratory compensation takes place rapidly.