26 : 26 Fluid, Electrolyte, and Acid-Base Balance
Body Water Content : Body Water Content Infants: 73% or more water (low body fat, low bone mass)
Adult males: ~60% water
Adult females: ~50% water (higher fat content, less skeletal muscle mass)
Water content declines to ~45% in old age
Fluid Compartments : Fluid Compartments Total body water = 40 L
Intracellular fluid (ICF) compartment: 2/3 or 25 L in cells
Extracellular fluid (ECF) compartment: 1/3 or 15 L
Plasma: 3 L
Interstitial fluid (IF): 12 L in spaces between cells
Other ECF: lymph, CSF, humors of the eye, synovial fluid, serous fluid, and gastrointestinal secretions
Slide 4: Figure 26.1 Total body water
Volume = 40 L
60% body weight Extracellular fluid (ECF)
Volume = 15 L
20% body weight Intracellular fluid (ICF)
Volume = 25 L
40% body weight Interstitial fluid (IF)
Volume = 12 L
80% of ECF
Composition of Body Fluids : Composition of Body Fluids Water: the universal solvent
Solutes: nonelectrolytes and electrolytes
Nonelectrolytes: most are organic
Do not dissociate in water: e.g., glucose, lipids, creatinine, and urea
Composition of Body Fluids : Composition of Body Fluids Electrolytes
Dissociate into ions in water; e.g., inorganic salts, all acids and bases, and some proteins
The most abundant (most numerous) solutes
Have greater osmotic power than nonelectrolytes, so may contribute to fluid shifts
Determine the chemical and physical reactions of fluids
Electrolyte Concentration : Electrolyte Concentration Expressed in milliequivalents per liter (mEq/L), a measure of the number of electrical charges per liter of solution
Extracellular and Intracellular Fluids : Extracellular and Intracellular Fluids Each fluid compartment has a distinctive pattern of electrolytes
ECF
All similar, except higher protein content of plasma
Major cation: Na+
Major anion: Cl–
Extracellular and Intracellular Fluids : Extracellular and Intracellular Fluids ICF:
Low Na+ and Cl–
Major cation: K+
Major anion HPO42–
Extracellular and Intracellular Fluids : Extracellular and Intracellular Fluids Proteins, phospholipids, cholesterol, and neutral fats make up the bulk of dissolved solutes
90% in plasma
60% in IF
97% in ICF
Slide 11: Figure 26.2 Na+ Sodium K+ Potassium Ca2+ Calcium Mg2+ Magnesium HCO3– Bicarbonate Cl– Chloride HPO42– SO42– Hydrogen
phosphate Sulfate Blood plasma Interstitial fluid Intracellular fluid
Fluid Movement Among Compartments : Fluid Movement Among Compartments Regulated by osmotic and hydrostatic pressures
Water moves freely by osmosis; osmolalities of all body fluids are almost always equal
Two-way osmotic flow is substantial
Ion fluxes require active transport or channels
Change in solute concentration of any compartment leads to net water flow
Slide 13: Figure 26.3 Lungs Interstitial
fluid Intracellular
fluid in tissue cells Blood
plasma O2 CO2 H2O,
Ions Nitrogenous
wastes Nutrients O2 CO2 H2O Ions Nitrogenous
wastes Nutrients Kidneys Gastrointestinal
tract H2O,
Ions
Water Balance and ECF Osmolality : Water Balance and ECF Osmolality Water intake = water output = 2500 ml/day
Water intake: beverages, food, and metabolic water
Water output: urine, insensible water loss (skin and lungs), perspiration, and feces
Slide 15: Figure 26.4 Feces 4% Sweat 8% Insensible losses
via skin and
lungs 28% Urine 60% 2500 ml Average output
per day Average intake
per day Beverages 60% Foods 30% Metabolism 10% 1500 ml 700 ml 200 ml 100 ml 1500 ml 750 ml 250 ml
Regulation of Water Intake : Regulation of Water Intake Thirst mechanism is the driving force for water intake
The hypothalamic thirst center osmoreceptors are stimulated by
Plasma osmolality of 2–3%
Angiotensin II or baroreceptor input
Dry mouth
Substantial decrease in blood volume or pressure
Regulation of Water Intake : Regulation of Water Intake Drinking water creates inhibition of the thirst center
Inhibitory feedback signals include
Relief of dry mouth
Activation of stomach and intestinal stretch receptors
Slide 18: Figure 26.5 (*Minor stimulus) Granular cells
in kidney Dry mouth Renin-angiotensin
mechanism Osmoreceptors
in hypothalamus Hypothalamic
thirst center Sensation of thirst;
person takes a
drink Water absorbed
from GI tract Angiotensin II Plasma osmolality Blood pressure Water moistens
mouth, throat;
stretches stomach,
intestine Plasma
osmolality Initial stimulus Result Reduces, inhibits Increases, stimulates Physiological response Plasma volume* Saliva
Regulation of Water Output : Regulation of Water Output Obligatory water losses
Insensible water loss: from lungs and skin
Feces
Minimum daily sensible water loss of 500 ml in urine to excrete wastes
Body water and Na+ content are regulated in tandem by mechanisms that maintain cardiovascular function and blood pressure
Regulation of Water Output: Influence of ADH : Regulation of Water Output: Influence of ADH Water reabsorption in collecting ducts is proportional to ADH release
ADH dilute urine and volume of body fluids
ADH concentrated urine
Regulation of Water Output: Influence of ADH : Regulation of Water Output: Influence of ADH Hypothalamic osmoreceptors trigger or inhibit ADH release
Other factors may trigger ADH release via large changes in blood volume or pressure, e.g., fever, sweating, vomiting, or diarrhea; blood loss; and traumatic burns
Slide 22: Figure 26.6 Osmolality
Na+ concentration
in plasma Stimulates Releases Osmoreceptors
in hypothalamus Negative
feedback
inhibits Posterior pituitary ADH Inhibits Stimulates Baroreceptors
in atrium and
large vessels Stimulates Plasma volume
BP (10–15%) Antidiuretic
hormone (ADH) Targets Effects Results in Collecting ducts
of kidneys Osmolality
Plasma volume Water reabsorption Scant urine
Disorders of Water Balance: Dehydration : Disorders of Water Balance: Dehydration Negative fluid balance
ECF water loss due to: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, diuretic abuse
Signs and symptoms: thirst, dry flushed skin, oliguria
May lead to weight loss, fever, mental confusion, hypovolemic shock, and loss of electrolytes
Slide 24: Figure 26.7a 1 2 3 Excessive
loss of H2O
from ECF ECF osmotic
pressure rises Cells lose
H2O to ECF
by osmosis;
cells shrink (a) Mechanism of dehydration
Disorders of Water Balance: Hypotonic Hydration : Disorders of Water Balance: Hypotonic Hydration Cellular overhydration, or water intoxication
Occurs with renal insufficiency or rapid excess water ingestion
ECF is diluted hyponatremia net osmosis into tissue cells swelling of cells severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral edema) possible death
Slide 26: Figure 26.7b 3 H2O moves
into cells by
osmosis; cells swell 2 ECF osmotic
pressure falls 1 Excessive
H2O enters
the ECF (b) Mechanism of hypotonic hydration
Disorders of Water Balance: Edema : Disorders of Water Balance: Edema Atypical accumulation of IF fluid tissue swelling
Due to anything that increases flow of fluid out of the blood or hinders its return
Blood pressure
Capillary permeability (usually due to inflammatory chemicals)
Incompetent venous valves, localized blood vessel blockage
Congestive heart failure, hypertension, blood volume
Edema : Edema Hindered fluid return occurs with an imbalance in colloid osmotic pressures, e.g., hypoproteinemia ( plasma proteins)
Fluids fail to return at the venous ends of capillary beds
Results from protein malnutrition, liver disease, or glomerulonephritis
Edema : Edema Blocked (or surgically removed) lymph vessels
Cause leaked proteins to accumulate in IF
Colloid osmotic pressure of IF draws fluid from the blood
Results in low blood pressure and severely impaired circulation
Electrolyte Balance : Electrolyte Balance Electrolytes are salts, acids, and bases
Electrolyte balance usually refers only to salt balance
Salts enter the body by ingestion and are lost via perspiration, feces, and urine
Electrolyte Balance : Electrolyte Balance Importance of salts
Controlling fluid movements
Excitability
Secretory activity
Membrane permeability
Table 26.1 Causes and Consequences of Electrolyte Imbalances (1 of 2) : Table 26.1 Causes and Consequences of Electrolyte Imbalances (1 of 2)
Table 26.1 Causes and Consequences of Electrolyte Imbalances (2 of 2) : Table 26.1 Causes and Consequences of Electrolyte Imbalances (2 of 2)
Central Role of Sodium : Central Role of Sodium Most abundant cation in the ECF
Sodium salts in the ECF contribute 280 mOsm of the total 300 mOsm ECF solute concentration
Na+ leaks into cells and is pumped out against its electrochemical gradient
Na+ content may change but ECF Na+ concentration remains stable due to osmosis
Central Role of Sodium : Central Role of Sodium Changes in plasma sodium levels affect
Plasma volume, blood pressure
ICF and IF volumes
Renal acid-base control mechanisms are coupled to sodium ion transport
Regulation of Sodium Balance : Regulation of Sodium Balance No receptors are known that monitor Na+ levels in body fluids
Na+-water balance is linked to blood pressure and blood volume control mechanisms
Regulation of Sodium Balance: Aldosterone : Regulation of Sodium Balance: Aldosterone Na+ reabsorption
65% is reabsorbed in the proximal tubules
25% is reclaimed in the loops of Henle
Aldosterone active reabsorption of remaining Na+
Water follows Na+ if ADH is present
Regulation of Sodium Balance: Aldosterone : Regulation of Sodium Balance: Aldosterone Renin-angiotensin mechanism is the main trigger for aldosterone release
Granular cells of JGA secrete renin in response to
Sympathetic nervous system stimulation
Filtrate osmolality
Stretch (due to blood pressure)
Regulation of Sodium Balance: Aldosterone : Regulation of Sodium Balance: Aldosterone Renin catalyzes the production of angiotensin II, which prompts aldosterone release from the adrenal cortex
Aldosterone release is also triggered by elevated K+ levels in the ECF
Aldosterone brings about its effects slowly (hours to days)
Slide 40: Figure 26.8 K+ (or Na+) concentration
in blood plasma* Stimulates Releases Targets Renin-angiotensin
mechanism Negative
feedback
inhibits Adrenal cortex Kidney tubules Aldosterone Effects Restores Homeostatic plasma
levels of Na+ and K+ Na+ reabsorption K+ secretion
Regulation of Sodium Balance: ANP : Regulation of Sodium Balance: ANP Released by atrial cells in response to stretch ( blood pressure)
Effects
Decreases blood pressure and blood volume:
ADH, renin and aldosterone production
Excretion of Na+ and water
Promotes vasodilation directly and also by decreasing production of angiotensin II
Slide 42: Figure 26.9 Stretch of atria
of heart due to BP Atrial natriuretic peptide (ANP) Adrenal cortex Hypothalamus
and posterior
pituitary Collecting ducts
of kidneys JG apparatus
of the kidney ADH release Aldosterone release Na+ and H2O reabsorption Blood volume Vasodilation Renin release* Blood pressure Releases Negative
feedback Targets Effects Effects Inhibits Effects Inhibits Results in Results in Angiotensin II
Influence of Other Hormones : Influence of Other Hormones Estrogens: NaCl reabsorption (like aldosterone)
H2O retention during menstrual cycles and pregnancy
Progesterone: Na+ reabsorption (blocks aldosterone)
Promotes Na+ and H2O loss
Glucocorticoids: Na+ reabsorption and promote edema
Cardiovascular System Baroreceptors : Cardiovascular System Baroreceptors Baroreceptors alert the brain of increases in blood volume and pressure
Sympathetic nervous system impulses to the kidneys decline
Afferent arterioles dilate
GFR increases
Na+ and water output increase
Slide 45: Figure 26.10 Stretch in afferent
arterioles Angiotensinogen
(from liver) Na+ (and H2O)
reabsorption Granular cells of kidneys Renin Posterior pituitary Systemic arterioles Angiotensin I Angiotensin II Systemic arterioles Vasoconstriction Aldosterone Blood volume Blood pressure Distal kidney tubules Adrenal cortex Vasoconstriction Peripheral resistance (+) (+) (+) (+) Peripheral resistance H2O reabsorption Inhibits baroreceptors
in blood vessels Sympathetic
nervous system ADH (antidiuretic
hormone) Collecting ducts
of kidneys Filtrate NaCl concentration in
ascending limb of loop of Henle Causes Causes Causes Causes Results in Secretes Results in Targets Results in Releases Release Catalyzes conversion Converting enzyme (in lungs) (+) (+) (+) (+) (+) (+) (+) stimulates Renin-angiotensin system Neural regulation (sympathetic
nervous system effects) ADH release and effects Systemic
blood pressure/volume
Regulation of Potassium Balance : Regulation of Potassium Balance Importance of potassium:
Affects RMP in neurons and muscle cells (especially cardiac muscle)
ECF [K+] RMP depolarization reduced excitability
ECF [K+] hyperpolarization and nonresponsiveness
Regulation of Potassium Balance : Regulation of Potassium Balance H+ shift in and out of cells
Leads to corresponding shifts in K+ in the opposite direction to maintain cation balance
Interferes with activity of excitable cells
Regulation of Potassium Balance : Regulation of Potassium Balance K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate
High K+ content of ECF favors principal cell secretion of K+
When K+ levels are low, type A intercalated cells reabsorb some K+ left in the filtrate
Regulation of Potassium Balance : Regulation of Potassium Balance Influence of aldosterone
Stimulates K+ secretion (and Na+ reabsorption) by principal cells
Increased K+ in the adrenal cortex causes
Release of aldosterone
Potassium secretion
Regulation of Calcium : Regulation of Calcium Ca2+ in ECF is important for
Neuromuscular excitability
Blood clotting
Cell membrane permeability
Secretory activities
Regulation of Calcium : Regulation of Calcium Hypocalcemia excitability and muscle tetany
Hypercalcemia Inhibits neurons and muscle cells, may cause heart arrhythmias
Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin
Influence of PTH : Influence of PTH Bones are the largest reservoir for Ca2+ and phosphates
PTH promotes increase in calcium levels by targeting bones, kidneys, and small intestine (indirectly through vitamin D)
Calcium reabsorption and phosphate excretion go hand in hand
Slide 53: Figure 16.12 Intestine Kidney Bloodstream Hypocalcemia (low blood Ca2+) stimulates
parathyroid glands to release PTH. Rising Ca2+ in
blood inhibits
PTH release. 1 PTH activates
osteoclasts: Ca2+
and PO43S released
into blood. 2 PTH increases
Ca2+ reabsorption
in kidney
tubules. 3 PTH promotes
kidney’s activation of vitamin D,
which increases Ca2+ absorption
from food. Bone Ca2+ ions PTH Molecules
Influence of PTH : Influence of PTH Normally 75% of filtered phosphates are actively reabsorbed in the PCT
PTH inhibits this by decreasing the Tm
Regulation of Anions : Regulation of Anions Cl– is the major anion in the ECF
Helps maintain the osmotic pressure of the blood
99% of Cl– is reabsorbed under normal pH conditions
When acidosis occurs, fewer chloride ions are reabsorbed
Other anions have transport maximums and excesses are excreted in urine
Acid-Base Balance : Acid-Base Balance pH affects all functional proteins and biochemical reactions
Normal pH of body fluids
Arterial blood: pH 7.4
Venous blood and IF fluid: pH 7.35
ICF: pH 7.0
Alkalosis or alkalemia: arterial blood pH >7.45
Acidosis or acidemia: arterial pH < 7.35
Acid-Base Balance : Acid-Base Balance Most H+ is produced by metabolism
Phosphoric acid from breakdown of phosphorus-containing proteins in ECF
Lactic acid from anaerobic respiration of glucose
Fatty acids and ketone bodies from fat metabolism
H+ liberated when CO2 is converted to HCO3– in blood
Acid-Base Balance : Acid-Base Balance Concentration of hydrogen ions is regulated sequentially by
Chemical buffer systems: rapid; first line of defense
Brain stem respiratory centers: act within 1–3 min
Renal mechanisms: most potent, but require hours to days to effect pH changes
Acid-Base Balance : Acid-Base Balance Strong acids dissociate completely in water; can dramatically affect pH
Weak acids dissociate partially in water; are efficient at preventing pH changes
Strong bases dissociate easily in water; quickly tie up H+
Weak bases accept H+ more slowly
Slide 60: Figure 26.11 (a) A strong acid such as
HCI dissociates
completely into its ions. (b) A weak acid such as
H2CO3 does not
dissociate completely. H2CO3 HCI
Chemical Buffer Systems : Chemical Buffer Systems Chemical buffer: system of one or more compounds that act to resist pH changes when strong acid or base is added
Bicarbonate buffer system
Phosphate buffer system
Protein buffer system
Bicarbonate Buffer System : Bicarbonate Buffer System Mixture of H2CO3 (weak acid) and salts of HCO3– (e.g., NaHCO3, a weak base)
Buffers ICF and ECF
The only important ECF buffer
Bicarbonate Buffer System : Bicarbonate Buffer System If strong acid is added:
HCO3– ties up H+ and forms H2CO3
HCl + NaHCO3 H2CO3 + NaCl
pH decreases only slightly, unless all available HCO3– (alkaline reserve) is used up
HCO3– concentration is closely regulated by the kidneys
Bicarbonate Buffer System : Bicarbonate Buffer System If strong base is added
It causes H2CO3 to dissociate and donate H+
H+ ties up the base (e.g. OH–)
NaOH + H2CO3 NaHCO3 + H2O
pH rises only slightly
H2CO3 supply is almost limitless (from CO2 released by respiration) and is subject to respiratory controls
Phosphate Buffer System : Phosphate Buffer System Action is nearly identical to the bicarbonate buffer
Components are sodium salts of:
Dihydrogen phosphate (H2PO4–), a weak acid
Monohydrogen phosphate (HPO42–), a weak base
Effective buffer in urine and ICF, where phosphate concentrations are high
Protein Buffer System : Protein Buffer System Intracellular proteins are the most plentiful and powerful buffers; plasma proteins are also important
Protein molecules are amphoteric (can function as both a weak acid and a weak base)
When pH rises, organic acid or carboxyl (COOH) groups release H+
When pH falls, NH2 groups bind H+
Physiological Buffer Systems : Physiological Buffer Systems Respiratory and renal systems
Act more slowly than chemical buffer systems
Have more capacity than chemical buffer systems
Respiratory Regulation of H+ : Respiratory Regulation of H+ Respiratory system eliminates CO2
A reversible equilibrium exists in the blood:
CO2 + H2O H2CO3 H+ + HCO3–
During CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O)
During CO2 loading the reaction shifts to the right (and H+ is buffered by proteins)
Respiratory Regulation of H+ : Respiratory Regulation of H+ Hypercapnia activates medullary chemoreceptors
Rising plasma H+ activates peripheral chemoreceptors
More CO2 is removed from the blood
H+ concentration is reduced
Respiratory Regulation of H+ : Respiratory Regulation of H+ Alkalosis depresses the respiratory center
Respiratory rate and depth decrease
H+ concentration increases
Respiratory system impairment causes acid-base imbalances
Hypoventilation respiratory acidosis
Hyperventilation respiratory alkalosis
Acid-Base Balance : Acid-Base Balance Chemical buffers cannot eliminate excess acids or bases from the body
Lungs eliminate volatile carbonic acid by eliminating CO2
Kidneys eliminate other fixed metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis
Renal Mechanisms of Acid-Base Balance : Renal Mechanisms of Acid-Base Balance Most important renal mechanisms
Conserving (reabsorbing) or generating new HCO3–
Excreting HCO3–
Generating or reabsorbing one HCO3– is the same as losing one H+
Excreting one HCO3– is the same as gaining one H+
Renal Mechanisms of Acid-Base Balance : Renal Mechanisms of Acid-Base Balance Renal regulation of acid-base balance depends on secretion of H+
H+ secretion occurs in the PCT and in collecting duct type A intercalated cells:
The H+ comes from H2CO3 produced in reactions catalyzed by carbonic anhydrase inside the cells
See Steps 1 and 2 of the following figure
Slide 74: Figure 26.12 1 CO2 combines with water
within the tubule cell,
forming H2CO3. 2 H2CO3 is quickly split,
forming H+ and bicarbonate
ion (HCO3–). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3– enters the
peritubular capillary blood either via symport
with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3– in the
filtrate, forming carbonic acid (H2CO3). HCO3–
disappears from the filtrate at the same rate
that HCO3– (formed within the tubule cell)
enters the peritubular capillary blood. 5 The H2CO3
formed in the
filtrate dissociates
to release CO2
and H2O. 6 CO2 diffuses
into the tubule
cell, where it
triggers further H+
secretion. * CA CO2 CO2
+
H2O 2K+ 2K+ * Na+ Na+ 3Na+ 3Na+ Tight junction H2CO3 H2CO3 PCT cell Nucleus Filtrate in
tubule lumen Cl– Cl– HCO3– + Na+ HCO3– H2O CO2 H+ H+ HCO3– HCO3– HCO3– ATPase ATPase Peri-
tubular
capillary 1 2 4 5 6 3a 3b Primary active
transport Simple diffusion Secondary active
transport Carbonic anhydrase Transport protein
Reabsorption of Bicarbonate : Reabsorption of Bicarbonate Tubule cell luminal membranes are impermeable to HCO3–
CO2 combines with water in PCT cells, forming H2CO3
H2CO3 dissociates
H+ is secreted, and HCO3– is reabsorbed into capillary blood
Secreted H+ unites with HCO3– to form H2CO3 in filtrate, which generates CO2 and H2O
HCO3– disappears from filtrate at the same rate that it enters the peritubular capillary blood
Slide 76: Figure 26.12 1 CO2 combines with water
within the tubule cell,
forming H2CO3. 2 H2CO3 is quickly split,
forming H+ and bicarbonate
ion (HCO3–). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3– enters the
peritubular capillary blood either via symport
with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3– in the
filtrate, forming carbonic acid (H2CO3). HCO3–
disappears from the filtrate at the same rate
that HCO3– (formed within the tubule cell)
enters the peritubular capillary blood. 5 The H2CO3
formed in the
filtrate dissociates
to release CO2
and H2O. 6 CO2 diffuses
into the tubule
cell, where it
triggers further H+
secretion. * CA CO2 CO2
+
H2O 2K+ 2K+ * Na+ Na+ 3Na+ 3Na+ Tight junction H2CO3 H2CO3 PCT cell Nucleus Filtrate in
tubule lumen Cl– Cl– HCO3– + Na+ HCO3– H2O CO2 H+ H+ HCO3– HCO3– HCO3– ATPase ATPase Peri-
tubular
capillary 1 2 4 5 6 3a 3b Primary active
transport Simple diffusion Secondary active
transport Carbonic anhydrase Transport protein
Generating New Bicarbonate Ions : Generating New Bicarbonate Ions Two mechanisms in PCT and type A intercalated cells
Generate new HCO3– to be added to the alkaline reserve
Both involve renal excretion of acid (via secretion and excretion of H+ or NH4+
Excretion of Buffered H+ : Excretion of Buffered H+ Dietary H+ must be balanced by generating new HCO3–
Most filtered HCO3– is used up before filtrate reaches the collecting duct
Excretion of Buffered H+ : Excretion of Buffered H+ Intercalated cells actively secrete H+ into urine, which is buffered by phosphates and excreted
Generated “new” HCO3– moves into the interstitial space via a cotransport system and then moves passively into peritubular capillary blood
Slide 80: Figure 25.13 Active
transport Passive
transport Peri-
tubular
capillary 2 4 4 3 3 1 1 2 4 3 Filtrate
in tubule
lumen Transcellular Paracellular Paracellular Tight junction Lateral intercellular space Capillary
endothelial
cell Luminal
membrane Solutes H2O Tubule cell Interstitial
fluid Transcellular Basolateral
membranes 1 Transport across the
luminal membrane. 2 Diffusion through the
cytosol. 4 Movement through the interstitial
fluid and into the capillary. 3 Transport across the basolateral
membrane. (Often involves the lateral
intercellular spaces because
membrane transporters transport ions
into these spaces.) Movement via the
transcellular route
involves: The paracellular route
involves: • Movement through
leaky tight junctions,
particularly in the PCT.
Ammonium Ion Excretion : Ammonium Ion Excretion Involves metabolism of glutamine in PCT cells
Each glutamine produces 2 NH4+ and 2 “new” HCO3–
HCO3– moves to the blood and NH4+ is excreted in urine
Slide 82: Figure 26.14 Nucleus PCT tubule cells Filtrate in
tubule lumen Peri-
tubular
capillary NH4+
out in urine 2NH4+ Na+ Na+ Na+ Na+ Na+ 3Na+ 3Na+ Glutamine Glutamine Glutamine Tight junction Deamination,
oxidation, and
acidification
(+H+) 2K+ 2K+ NH4+ HCO3– 2HCO3– HCO3–
(new) ATPase 1 PCT cells metabolize glutamine to
NH4+ and HCO3–. 2a This weak acid NH4+ (ammonium) is
secreted into the filtrate, taking the
place of H+ on a Na+- H+ antiport carrier. 2b For each NH4+ secreted, a
bicarbonate ion (HCO3–) enters the
peritubular capillary blood via a
symport carrier. 3 The NH4+ is excreted in the urine. Primary
active
transport Simple
diffusion Secondary
active
transport Transport
protein 1 2a 2b 3
Bicarbonate Ion Secretion : Bicarbonate Ion Secretion When the body is in alkalosis, type B intercalated cells
Secrete HCO3–
Reclaim H+ and acidify the blood
Bicarbonate Ion Secretion : Bicarbonate Ion Secretion Mechanism is the opposite of the bicarbonate ion reabsorption process by type A intercalated cells
Even during alkalosis, the nephrons and collecting ducts excrete fewer HCO3– than they conserve
Abnormalities of Acid-Base Balance : Abnormalities of Acid-Base Balance Respiratory acidosis and alkalosis
Metabolic acidosis and alkalosis
Respiratory Acidosis and Alkalosis : Respiratory Acidosis and Alkalosis The most important indicator of adequacy of respiratory function is PCO2 level (normally 35–45 mm Hg)
PCO2 above 45 mm Hg respiratory acidosis
Most common cause of acid-base imbalances
Due to decrease in ventilation or gas exchange
Characterized by falling blood pH and rising PCO2
Respiratory Acidosis and Alkalosis : Respiratory Acidosis and Alkalosis PCO2 below 35 mm Hg respiratory alkalosis
A common result of hyperventilation due to stress or pain
Metabolic Acidosis and Alkalosis : Metabolic Acidosis and Alkalosis Any pH imbalance not caused by abnormal blood CO2 levels
Indicated by abnormal HCO3– levels
Metabolic Acidosis and Alkalosis : Metabolic Acidosis and Alkalosis Causes of metabolic acidosis
Ingestion of too much alcohol ( acetic acid)
Excessive loss of HCO3– (e.g., persistent diarrhea)
Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure
Metabolic Acidosis and Alkalosis : Metabolic Acidosis and Alkalosis Metabolic alkalosis is much less common than metabolic acidosis
Indicated by rising blood pH and HCO3–
Caused by vomiting of the acid contents of the stomach or by intake of excess base (e.g., antacids)
Effects of Acidosis and Alkalosis : Effects of Acidosis and Alkalosis Blood pH below 7 depression of CNS coma death
Blood pH above 7.8 excitation of nervous system muscle tetany, extreme nervousness, convulsions, respiratory arrest
Respiratory and Renal Compensations : Respiratory and Renal Compensations If acid-base imbalance is due to malfunction of a physiological buffer system, the other one compensates
Respiratory system attempts to correct metabolic acid-base imbalances
Kidneys attempt to correct respiratory acid-base imbalances
Respiratory Compensation : Respiratory Compensation In metabolic acidosis
High H+ levels stimulate the respiratory centers
Rate and depth of breathing are elevated
Blood pH is below 7.35 and HCO3– level is low
As CO2 is eliminated by the respiratory system, PCO2 falls below normal
Respiratory Compensation : Respiratory Compensation Respiratory compensation for metabolic alkalosis is revealed by:
Slow, shallow breathing, allowing CO2 accumulation in the blood
High pH (over 7.45) and elevated HCO3– levels
Renal Compensation : Renal Compensation Hypoventilation causes elevated PCO2
(respiratory acidosis)
Renal compensation is indicated by high HCO3– levels
Respiratory alkalosis exhibits low PCO2 and high pH
Renal compensation is indicated by decreasing HCO3– levels
Table 26.2 Causes and Consequences of Acid-Base Imbalances (1 of 2) : Table 26.2 Causes and Consequences of Acid-Base Imbalances (1 of 2)
Table 26.2 Causes and Consequences of Acid-Base Imbalances (2 of 2) : Table 26.2 Causes and Consequences of Acid-Base Imbalances (2 of 2)