chapt27_lecture10e.ppt

27-1

Chapter 27

Water, Electrolytes, and

Acid-Base Balance

27-2

27.1 Body Fluids

• Intracellular fluid compartment– All fluids inside cells of body– About 40% of total body weight

• Extracellular fluid compartment– All fluids outside cells– About 20% of total body weight– Subcompartments

• Interstitial fluid and plasma; lymph, CSF, synovial fluid• Primary intracellular ions, interstitial fluid ions, and plasma ions

– Intracellular cation = K+

– Interstitial fluid cation = Na+

– Plasma cation = Na+

– Intracellular anion = Phosphate– Interstitial fluid = Cl-

– Plasma anion = Cl-

27-3

Body Fluid Compartments

Approximate Concentration of major Solutes in Body Fluids*

Intracellular Fluid†

Phosphate (HPO42− plus HPO4

−)

*Expressed as milliequivalents per liter (meq/l).†Data are from skeletal muscle.

Interstitial FluidPlasma

TABLE 27.2

SoluteCations

Sodium (Na+)

Potassium (K+)

Calcium (Ca2+)

Magnesium (Mg2+)

TOTAL

Anions

Chloride (Cl–)

Bicarbonate (HCO3–)

Protein

Other

TOTAL

153.2

4.3

3.8

1.4

145.1

4.1

3.4

1.3

12.0

150.0

4.0

34.0

153.9

118.0

27.0

2.3

0.0

6.6

153.9 200.0

90.0

54.0

40.0

12.0

4.0

200.0

162.7

6.3

17.0

2.2

25.7

111.5

162.7

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

27-4

27.2 Regulation of Body Fluid Concentration and Volume

• Content regulated so total volume of water in body remains constant

• Kidneys are primary regulators of water excretion

• Regulation processes– Osmosis– Osmolality– Baroreceptors– Learned behavior

• Sources of water– Ingestion

– Cellular metabolism

• Routes of water loss– Urine

– Evaporation• Perspiration

• Respiratory passages

– Feces

27-5

Extracellular Fluid Osmolality• Osmolality

– Measure of water vs. solute concentration; the higher the solute concentration, the higher the osmolality

– Adding or removing water from a solution changes osmolality

• Increased osmolality: triggers thirst and ADH secretion

• Decreased osmolality: inhibits thirst and ADH secretion

27-6


3

1 Baroreceptorsin heart

2 Juxtaglomerularapparatuses in kidney

1 The baroreceptors in the carotid sinuses and aortic arch detect reduced bloodpressure, which signals the hypothalamic thirst center.

2 Simultaneously, the juxtaglomerular apparatuses detect low blood pressure, whichactivates the renin-angiotensin system to produce angiotensin II. Angiotensin IIstimulates the hypothalamic thirst center.

3 Osmoreceptors in the hypothalamus shrink when blood osmolality goes up,triggering action potentials that stimulate thirst.

4 The combination of these inputs activates thirst and promotes water consumption.

Osmoreceptors inhypothalamus(increased osmolality)

4 Increasedthirst

27-7

Hormonal Regulation of Blood OsmolalityCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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Osmoreceptors in the hypothalamuscontrol center detect the increase in blood osmolality and signal the posteriorpituitary to secrete ADH, whichcauses thirst. ADH also increases thepermeability of the distal convolutedtubule and collecting ducts to water.

Water reabsorption at the distalconvoluted tubule and collectingduct increases; water consumptionincreases .

Blood osmolality increases:Homeostasis Disturbed

Blood osmolality decreases:Homeostasis Restored

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Blood osmolality decreases:Homeostasis Disturbed

Blood osmolality increases:Homeostasis Restored

Osmoreceptors in the hypothalamusdetect the decrease in bloodosmolality and signal the posteriorpituitary to reduce ADH secretion,which decreases thirst.

Water reabsorption at the distalconvoluted tubule and collectingduct decreases; waterconsumption decreases.

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Control Center

Effectors Activated:

Control CenterEffectors Activated:

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27-8

Regulation of ECF Volume• ECF can increase or decrease even if osmolality of

extracellular fluid is maintained• Carotid sinus and aortic arch baroreceptors monitor blood

pressure, juxtaglomerular apparatuses monitor pressure changes, receptors in walls of atria and large vessels respond to small changes in BP

• These receptors activate these mechanisms– Neural: increase in BP recognized by baroreceptors. Decreased

sympathetic stimulation of afferent arteriole leads to increased pressure in glomerulus leading to increased filtration and increased urine output.

– Renin-angiotensin-aldosterone– Atrial natriuretic hormone (ANH)– Antidiuretic hormone (ADH)

27-9

Regulation of Blood VolumeCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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Pituitary:Baroreceptors stimulate posterior pituitary ADH secretionwhen blood volume decreases. Increased ADH alsoincreases the sensation of thirst.

Increased aldosterone and decreased ANH increase

Na+ reabsorption in the distal convoluted tubule and thecollecting duct. Less Na+ and water are excreted in theurine.

Increased ADH increases the permeability of the distal convoluted tubule and the collecting duct to water. Less water is excreted in urine.

Decreased renal blood flow decreases filtrate formation,and less water is excreted in urine.

Decreased aldosterone and increased ANH decrease

Na+ reabsorption into the distal convoluted tubule andcollecting duct. More Na+ in urine, which decreases blood volume

Decreased ADH decreases water reabsorption by thedistal convoluted tubules and collecting ducts. Lesswater returns to the blood, and more water is excreted in the urine.

Blood vessels:Sympathetic division baroreceptors detect increased bloodvolume, which causes vasodilation of renal arteries.

Heart:Atrial cardiac muscle cells secrete ANH when bloodvolume increases.

Kidney:Juxtaglomerular apparatuses inhibit renin release whenblood volume increases, which decreasesaldoster one secretion.

Pituitary:Baroreceptors inhibit posterior pituitary ADH secretionwhen blood volume increases.


Increased renal blood flow increases the rate of filtrateformation, and more water is excreted in the urine.

High blood volume induces elevated bloodpressure: Homeostasis Disturbed

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Low blood volume induces lowered bloodpressure: Homeostasis Disturbed

Reduced blood volume due to loss of water

and Na+ in the urine lowers blood pressure:Homeostasis Restored

Increased blood volume due to decreased Na+ and water loss in the urine raises blood pressure:

Homeostasis Restored

Blood vessels:Sympathetic division baroreceptors detect decreasedblood volume, which causes vasoconstriction of renalarteries.

Heart:Atrial cardiac muscle cells do not secrete ANH whenblood volume decreases.

Kidney:Juxtaglomerular apparatuses stimulate renin releasewhen blood volume decreases, which increasesaldosterone secretion.

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27-10

Regulation of ECF VolumeCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

DecreasedBP

Kidney

Increased Na+

and waterreabsorptionresults inincreased BP.

Increasedrenin secretion(from kidney)

Angiotensinogen

Angiotensin I

Angiotensin II

Increasedaldosterone secretion

Increased BPin right atrium

ANH

Kidney

Increased ANH Increased Na+

excretion andincreased waterloss result indecreased BP.

27-11

Regulation of ECF Osmolality

• Electrolytes– Molecules or ions with an

electrical charge• Ingestion adds electrolytes to

body• Kidneys, liver, skin, lungs

remove from body– Concentration changes only

when growing, gaining or losing weight

• Na+ Ions– Dominant ECF cations– Responsible for 90-95% of

osmotic pressure

• Regulation of Na+ ions– Kidneys major route of

excretion– Small quantities lost in sweat

{sweat = (in decreasing amounts) water, Na+, urea, Cl-

K+, NH3}. Insensible perspiration is water evaporating from skin. Sensible perspiration is secreted by the sweat glands. Contains solutes

• Terms– Hypernatremia: elevated

plasma Na+ – Hyponatremia: decreased

Na+

27-12

27.3 Regulation of ICF


1

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Large organic molecules, such as proteins,which cannot cross the plasma membrane,are synthesized inside cells and influencethe concentration of solutes inside the cells.

The transport of ions, such as Na+, K+, andCa2+, across the plasma membrane influencesthe concentration of ions inside and outsidethe cell.

An electrical charge difference across theplasma membrane influences the distributionof ions inside and outside the cell.

The distribution of water inside and outside thecell is determined by osmosis.

Large organicmolecules

Extracellular fluid

Intracellularfluid

Water moves by osmosis.

Electrical chargedifference

Ion transport(e.g., Na+, K+, Ca2+)

H2 O

(e.g., K+)

27-13

27.4 Regulation of Specific Electrolytes

• Chloride ions– Predominant anions in ECF

• Magnesium ions– Capacity of kidney to

reabsorb is limited

– Excess lost in urine

– Decreased extracellular magnesium results in greater degree of reabsorption

• Potassium ions– Maintained in narrow range

– Affect resting membrane potentials

– Aldosterone increases amount secreted

• Terms– Hyperkalemia: abnormally

high levels of potassium in extracellular fluid

– Hypokalemia: abnormally low levels of potassium in extracellular fluid.

27-14

Table 27.5 Homeostasis: Mechanisms Regulating Blood Sodium

Response to Changes in Blood Osmolality

Antidiuretic hormone(ADH); the mostimportant regulatorof blood osmolality

Increased bloodosmolality (e.g.,increased Na+

concentration)

Increased ADH secretionfrom the posterior pituitary;mediated through cells inthe hypothalamus

Increased water reabsorptionin the kidney; productionof a small volume ofconcentrated urine

Decreased blood osmolalityas reabsorbed water dilutesthe blood

Decreased bloodosmolality (e.g.,decreased Na+

concentration)

Decreased ADH secretionfrom the posterior pituitary;mediated through cells inthe hypothalamus

Decreased water reabsorptionin the kidney; production of alarge volume of dilute urine

Increased blood osmolalityas water is excreted fromthe blood into the urine

Response to Changes in Blood Pressure

Renin-angiotensinaldosteronehormonemechanism

Decreased bloodpressure in the kidney’safferent arterioles

Increased renin releasefrom the juxtaglomerularapparatuses; renininitiates the conversionof angiotensinogen toangiotensin; angiotensin Iis converted toangiotensin II, which increasesaldosterone secretion fromthe adrenal cortex

Increased Na+ reabsorptionin the kidney (because ofincreased aldosterone);increased water reabsorptionas water follows the Na+;decreased urine volume

Increased blood pressureas blood volume increasesbecause of increased waterreabsorption; bloodosmolality is maintainedbecause both Na+ andwater are reabsorbed*

Increased bloodpressure in the kidney’safferent arterioles

Decreased renin releasefrom the juxtaglomerularapparatuses, resulting inreduced formation ofangiotensin I; reducedangiotensin I leads toreduced angiotensin II,which causes a decreasein aldosterone secretionfrom the adrenal cortex

Decreased Na+ reabsorptionin the kidney (because ofdecreased aldosterone);decreased water reabsorptionas less Na+ is reabsorbed;increased urine volume

Decreased blood pressureas blood volume decreasesbecause water is excreted inthe urine; blood osmolalityis maintained because bothNa+ and water are excretedin the urine*

Atrial natriuretichormone (ANH)

Decreased bloodpressure in theatria of the heart

Decreased ANH releasedfrom the atria

Increased Na+ reabsorptionin the kidney; increasedwater reabsorption as waterfollows the Na+; decreasedurinary volume

Increased blood pressureas blood volume increasesbecause of increased waterreabsorption; bloodosmolality is maintainedbecause both Na+ andwater are reabsorbed*

Increased bloodpressure in theatria of the heart

Increased ANH releasedfrom the atria

Decreased Na+ reabsorptionin the kidney; decreasedwater reabsorption aswater is excreted with Na+

in the urine; increasedurinary volume

Decreased blood osmolalityas blood volume decreasesbecause water is excreted inthe urine; blood osmolalityis maintained because bothNa+ and water are excretedin the urine*

ADH—activated bysignificant decreasesin blood pressure;normally regulates bloodosmolality (see above)

Decreased arterialblood pressure

Increased ADH secretionfrom the posteriorpituitary; mediatedthrough baroreceptors

Increased water reabsorptionin the kidney; productionof a small volume ofconcentrated urine

Increased blood pressureresulting from increasedblood volume; decreasedblood osmolality

Increased arterialblood pressure

Decreased ADH secretionfrom the posteriorpituitary; mediatedthrough baroreceptors

Decreased water reabsorptionin the kidney; production of alarge volume of dilute urine

Decreased blood pressureresulting from decreasedblood volume; increasedblood osmolality

Abbreviation: A DH = antidiuretic hormone.*Assumes normal levels of A DH.

Mechanism Stimulus Response to Stimulus Effect of Response Result


27-15

Consequences of AbnormalPlasma Levels of Sodium Ions

Lethargy, confusion, apprehension, seizures, and coma

When accompanied by reduced blood volume:reduced blood pressure, tachycardia, and decreasedurine output

When accompanied by increased blood volume:weight gain, edema, and distension of veins

High dietary sodium (rarely causes symptoms)

Administration of hypertonic saline solutions

Oversecretion of aldosterone

Thirst, fever, dry mucous membranes, and restlessness

Most serious symptoms are convulsions andpulmonary edema

When occurring with increased water volume:weight gain, edema, elevated blood pressure,and bounding pulse

TABLE 27.6

Causes Inadequatedietary intake of sodium

Extrarenal losses

Dilution

Hyperglycemia

Symptoms

HYPERNATREMIA

Causes

Symptoms

Water loss


HYPONATREMIA

27-16

Potassium Ion Regulation in ECFCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Blood K+ levels increase:Homeostasis Disturbed

Blood K+ levels decrease:Homeostasis Disturbed

Blood K+ levels decrease:Homeostasis Restored

Blood K+ levels increase:Homeostasis Restored

Decreased blood levels of K+ acton the adrenal cortex to decreasealdosterone secretion

Decreased aldosterone reduces the

rate of K+ secretion from the distalconvoluted tubules and collectingducts of the kidneys into the urine.

Increased blood levels of K+ acton the adrenal cortex to increasealdosterone secretion.

Elevated aldosterone increases the

rate of K+ secretion from the distalconvoluted tubules and collectingducts of the kidney into the urine.

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27-17

Consequences of AbnormalConcentrations of Potassium Ions

Loss of intracellular K+ due to cell trauma orreduced permeability of plasma membrane

Reduced renal excretion

Increased neuromuscular irritability

Intestinal cramping and diarrhea

Rapid cardiac repolarization

Loss of muscle tone and paralysis

Reduced rate of cardiac action potential conduction

TABLE 27.7

HYPOKALEMIA

Causes

Symptoms

Causes

Symptoms

Mild

Severe Muscle weakness

HYPERKALEMIA

Atrioventricular block

Delayed ventricular depolarization

Bradycardia

Decreased smooth muscle tone

Decreased neuromuscular excitability

Increased renalloss

Reduced K– intake

Alkalosis

Insulin administration


27-18

Regulation of Calcium Ions

• Regulated within narrow range– Elevated extracellular

levels prevent membrane depolarization

– Decreased levels lead to spontaneous action potential generation

• Terms– Hypocalcemia– Hypercalcemia

• PTH increases Ca2+ extracellular levels and decreases extracellular phosphate levels

• Vitamin D stimulates Ca2+ uptake in intestines

• Calcitonin decreases extracellular Ca2+ levels

27-19

Consequences of AbnormalConcentrations of Calcium Ions

Nutritional deficiencies

Vitamin D deficiency

Decreased parathyroid hormone secretion

Malabsorption of fats (reduces vitamin D absorption)

Bone tumors that increase Ca2+ deposition

Reduced cardiac ventricular depolarization

TABLE 27.8

HYPOCALCEMIA

Causes

Symptoms Confusion

Muscles pasmsa

Hyperreflexi

Intestinal cramping

Convulsions

Tetany

Inadequate respiratory movements

Prolonged cardiac ventricular depolarization

HYPERCALCEMIA

Excessive parathyroid hormone secretion

Excess vitamin D

Fatigue

Weakness

Causes

Symptoms

Anorexia

Lethargy

Nausea

Constipation

Kidney stones


27-20

Regulation of Magnesium IonsCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Decreased blood Mg2+ levelscause the kidneys to reabsorbmost of the Mg2+ from the filtrate.

Less Mg2+ enters the urine, and the

blood Mg2+ level is maintained.

Increased blood Mg2+ levels inthe filtrate exceed the kidney'scapacity to reabsorb Mg2+ fromthe filtrate.

The Mg2+ not reabsorbed from thefiltrate enter the urine.

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Blood Mg2+ levels increase:Homeostasis Disturbed

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Blood Mg2+ levels decrease:Homeostasis Disturbed

Blood Mg2+ levels increase:Homeostasis Restored

Blood Mg2+ levels decrease:Homeostasis Restored



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27-21

Consequences of AbnormalConcentrations of Magnesium Ions

Reduced magnesium intestinal absorption

Renal tubular dysfunction

TABLE 27.9

HYPOMAGNESEMIA (rare)

Malnutrition

Alcoholism

Causes

Symptoms

Some diuretics

Irritability

Muscle weakness

Tetany

Convulsions

HYPERMAGNESEMIA (rare)

Renal failure

Magnesium-containingant acids

Nausea

Vomiting

Muscle weakness

Hypotension

Bradycardia

Reduced respiration

Causes

Symptoms


27-22

Regulation of Blood Phosphate ionCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Decreased blood PO43– levels

cause the kidneys to reabsorbmost of the PO4

3– from thefiltrate.

Less PO43– enter the urine and the blood

PO43– level is maintained.

Increased blood PO43– levels

cause the PO43– levels in the

filtrate to exceed the kidney’scapacity to reabsorb PO4

3– fromthe filtrate.

The PO43– not reabsorbed from the filtrate

enter the urine.

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Blood PO43– levels increase:

Homeostasis Disturbed

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Blood PO43– levels decrease:

Homeostasis Disturbed

Blood PO43– levels decrease:

Homeostasis DisturbedBlood PO4

3– levels increase:Homeostasis Disturbed



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27-23

Regulation of Phosphate Ions

• Under normal conditions, reabsorption of phosphate occurs at maximum rate in the nephron

• An increase in plasma phosphate increases amount of phosphate in nephron beyond that which can be reabsorbed; excess is lost in urine

– Hypophosphatemia: reduced absorption from intestine due to vitamin D deficiency or alcohol abuse.

– Hyperphosphatemia: renal failure, chemotherapy, hyperparathyroidism (secondary to elevated plasma calcium levels)

27-24

Reduced intestinal absorption due to vitamin Ddeficiency or alcohol abuse

Hyperparathyroidism (reduced renal PO4− excretion)

Formation of calcium phosphate deposits in tissuesof lungs, kidneys and joints

TABLE 27.10 Consequences of AbnormalConcentrations of Phosphate Ions

HYPOPHOSPHATEMIA

Causes

Symptoms

Causes

Symptoms

Symptoms of reduced Ca2+ related to formationof deposits

Renal failure

Tissue destruction from chemotherapy

Reduced blood clotting

Reduced white blood cell functions

Reduced oxygentransport

Reduced metabolicrate

Hyperparathyroidism (elevatedrenal PO4– excretion)


HYPERPHOSPHATEMIA

27-25

Comparison of Strong and Weak Acids

Hydrochloric acidHCI

Hydrogen ionH+

Chloride ionCI–

(complete dissociation)

+

Carbonic acidH2CO3

Hydrogen ion Bicarbonate ion+

Equilibrium

Strong baseNaOH Na+ OH–

Sodium hydroxide Sodium ion Hydroxide ion

+

(partial dissociation)

(complete dissociation)

Strong acid

Weak acidH+ HCO3

–


27-26

27.5 Regulation of Acid-Base Balance

• Acids– Release H+ into

solution

• Bases– Remove H+ from

solution

• Acids and bases– Grouped as strong or

weak

• Buffers: Resist changes in pH– When H+ added, buffer

removes it– When H+ removed, buffer

replaces it

• Types of buffer systems– Carbonic acid/bicarbonate– Protein– Phosphate

27-27

Regulation of Acid-Base Balance

Blood pH increases (H+ decreases):Homeostasis Disturbed

Blood pH decreases (H+ increases):Homeostasis Restored

Kidney:The distal convoluted tubules

decrease H+ secretion into the urine

and decrease HCO3– reabsorption into

the blood.

Lungs:The respiratory center in the braindecreases the rate and depth ofbreathing, which increases blood CO2.

Kidney:

Fewer H+ are removed from the blood,

and fewer HCO3– are available to bind

to H+

Lungs:Increased blood CO2 reacts withwater to produce carbonic acid,

which dissociates to increase H+.

H2O + CO2 H2CO3 H+ + HCO3–

Lungs:The respiratory center in the brainincreases the rate and depth ofbreathing, which decreases blood CO2.

Actions

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Buffers:

Buffers release H+.

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Buffers:

The number of H+ in the blood increases.


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Blood pH decreases (H+ increases):Homeostasis Disturbed

Blood pH decreases (H+ decreases):Homeostasis Disturbed


Buffers:

Buffers bind H.

Kidney:The distal convoluted tubules

increase H+ secretion into the urine

and increase HCO3– reabsorption into

the blood.

Lungs:

Decreased blood CO2 causes H+

react with HCO3– to form carbonic acid,

which decreases H+ in blood.H2O + CO2 H2CO3 H+ + HCO3

–

Buffers:

The number of H+ in the blood decreases.

Reactions

Kidney:

Fewer H+ are removed from the blood,

and fewer HCO3– are available to bind

to H+



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27-28

Regulation of Acid/Base Balance• Buffers: if pH rises, buffers bind H+; if pH falls,

buffers release H+

– Protein buffer: Intracellular and plasma proteins absorb H+. Provide ¾ of buffering in body. E.g., hemoglobin.

– Bicarbonate buffering system: Important in plasma– Phosphate buffer system: important as an intracellular

buffer• Respiratory center: if pH rises, respiratory rate

decreases; if pH falls, respiratory rate increases• Kidneys: if pH rises, distal tubule decreases H+

secretion into the urine and decreases HCO3-

absorption into the blood (more H2CO3 will dissociate into H+ and HCO3

-); if pH falls, distal tubule increases H+ secretion into the urine and increases HCO3

- absorption into the blood

27-29

Carbonic acid/bicarbonatebuffer system

Components of the carbonic acid/bicarbonate buffer system are not present in high enough concentrations in the extracellularfluid to constitute a powerful buffer system. However, the concentrations of the components of the buffer system are regulated.Therefore, it plays an exceptionally important role in controlling the pH of extracellular fluid.

Intracellular proteins and plasma proteins form a large pool of protein molecules that can act as buffer molecules. Because oftheir high concentration, they provide approximately three-fourths of the body’s buffer capacity. Hemoglobin in red blood cells isan important intracellular protein. Other intracellular molecules, such as histone proteins and nucleic acids, also act as buffers.

Components of the phosphate buffer system are low in the extracellular fluids, compared with the other buffer systems, but it isan important intracellular buffer system.

Protein buffer system

Phosphate buffersystem

Characteristics of Buffer SystemsTABLE 27.11


27-30

Respiratory Regulation ofAcid-Base Balance

• Achieved through carbonic acid/bicarbonate buffer system– As carbon dioxide levels increase, pH decreases

– As carbon dioxide levels decrease, pH increases

– Carbon dioxide levels and pH affect respiratory centers

• Hypoventilation increases blood carbon dioxide levels

• Hyperventilation decreases blood carbon dioxide levels

27-31



Circulation

Carbonican hydrase

Capillary

11

2

3

2

3

Carbon dioxide reacts with H2O toform H2CO3. An enzyme, carbonicanhydrase, found in red blood cellsand on the surface of blood vesselepithelium, catalyzed the reaction.Carbonic acid dissociates to formH+ and HCO3

–. An equilibrium isquickly established.

Decreased pH in the extracellularfluid stimulates the respiratorycenter and causes an increasedrate and depth of breathing.

Increased rate and depth ofbreathing causes CO2 to beexpelled from the lungs, thusreducing the extracellular CO2

levels. As CO2 levels decrease,theextracellular concentration of H+

decreases, and the extracellularfluid pH increases.

DecreasedpH

Respiratorycenter in

brainstem

Lungs

Increasedrespiratory rate

and depth

Increased CO2

expelled from the lungs

27-32

Renal Regulation of Acid-Base Balance

• Secretion of H+ into filtrate and reabsorption of HCO3

- into ECF cause extracellular pH to increase

• HCO3- in filtrate reabsorbed

• Rate of H+ secretion increases as body fluid pH decreases or as aldosterone levels increase

• Secretion of H+ inhibited when urine pH falls below 4.5

27-33

Renal Regulation ofAcid-Base Balance

CO2Lumen

Na+

4

When the filtrate or blood pH

decreases, H+ combine with HCO3–

to form carbonic acid that is convertedinto CO2 and H2O. The CO2 diffusesinto tubule cells.

In the tubule cells, CO2 combines withH2O to form H2CO3 that dissociates to

form H+ and HCO3.

An antiport mechanism secretes H+ intothe filtrate in exchange for Na+ from thefiltrate. As a result, filtrate pH decreases.

Bicarbonate ions are symported withNa+ into the interstitial fluid. They thendiffuse into capillaries.

In capillaries, HCO3– combine with H+.This decreases the H+ concentrationand increases blood pH.

1

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5

3

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3

4

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Peritubularcapillary

Interstitialfluid

Basalmembrane

Tubule cellcytoplasmApicalmembrane

CO2

CO2 + H2O H2CO3

Na+

H+

Symport

Antiport

H+ HCO3–+


+ H2O H2CO3 H+ + HCO3

– HCO3– + Na+

27-34

Hydrogen Ion BufferingCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

1 2

3

4

Lumen

Na+

Na+

Hydrogen ions can react with HCO3–

that enters the filtrate to form H2CO3,which is in equilibrium with H2O andCO2.

Hydrogen ions can react with HPO42–

that enters the filtrate to form H2PO4–.

Hydrogen ions can react with NH3 to

form NH4+.

1

2

3

4

Hydrogen ions secreted into thefiltrate are buffered.

InterstitialfluidBasalmembrane

Tubule cellcytoplasm

Apicalmembrane

Symport

Antiport

HCO3– + H+ H3CO3 H2O + CO2

NaHCO3Fromfiltrate Na2HPO4

NH3 NH3 +

+ HCO3–

Na+ + HCO3– H2CO3 H2O ++ H+ CO2

2 Na+ + HPO42– + H+ Na+ + H2PO4

2–

H+ NH4+

27-35

Acidosis and Alkalosis• Acidosis: pH body fluids below 7.35

– Respiratory: Caused by inadequate ventilation- reduced elimination of CO2, asthma, damage to respiratory center in brain, emphysema.

– Metabolic: Results from all conditions other than respiratory that decrease pH- diarrhea, vomiting, ingesting overdose of aspirin, untreated diabetes mellitus, anaerobic respiration

• Alkalosis: pH body fluids above 7.45– Respiratory: Caused by hyperventilation, high altitude (reduced

partial pressure of O2

– Metabolic: Results from all conditions other than respiratory that increase pH- severe vomiting, too much aldosterone, ingestion of substances like bicarbonate of soda.

• Compensatory mechanisms

27-36

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