Chapter 20b

Report
Chapter 20b
Integrative
Physiology II:
Fluid and Electrolyte
Balance
Potassium Balance
• Regulatory mechanisms keep plasma
potassium in narrow range
• Aldosterone plays a critical role
• Hypokalemia
• Muscle weakness and failure of respiratory
muscles and the heart
• Hyperkalemia
• Can lead to cardiac arrhythmias
• Causes include kidney disease, diarrhea, and
diuretics
Behavioral Mechanisms
• Drinking replaces fluid loss
• Low sodium stimulates salt appetite
• Avoidance behaviors help prevent
dehydration
• Desert animals avoid the heat
Disturbances in Volume and Osmolarity
Figure 20-16
Volume and Osmolarity
Table 20-1 (1 of 3)
Volume and Osmolarity
Table 20-1 (2 of 3)
Volume and Osmolarity
Table 20-1 (3 of 3)
Volume and Osmolarity
• Homeostatic
compensation
for severe
dehydration
Blood volume/
Blood pressure
DEHYDRATION
CARDIOVASCULAR
MECHANISMS
accompanied by
RENAL
MECHANISMS
RENIN-ANGIOTENSIN
SYSTEM
+
Carotid and aortic
baroreceptors
+
+
Granular
cells
CVCC
Flow at
macula densa
HYPOTHALAMIC
Hypothalamic
MECHANISMS
osmoreceptors
Atrial volume
receptors; Carotid
and aortic
baroreceptors
+
+
Volume
conserved
Renin
Angiotensinogen
Parasympathetic
output
GFR
Osmolarity
Sympathetic
output
Hypothalamus
+
ANG I
Vasopressin
release from
posterior pituitary
ACE
+
+
+
Heart
+
Arterioles
ANG II
Thirst
+
Adrenal
cortex
Vasoconstriction
Rate
osmolarity inhibits
Force
Aldosterone
Peripheral
resistance
Distal
nephron
Distal
nephron
Na+
reabsorption
Cardiac
output
Blood
pressure
H2O
and
reabsorption
Volume
H2O
intake
Osmolarity
Figure 20-17
Volume and Osmolarity
Blood volume/
Blood pressure
DEHYDRATION
accompanied by
Osmolarity
RENAL
MECHANISMS
RENIN-ANGIOTENSIN
SYSTEM
+
+
+
Granular
cells
CVCC
Flow at
macula densa
+
Volume
conserved
Renin
Angiotensinogen
Parasympathetic
output
GFR
+
Sympathetic
output
ANG I
Vasopressin
release from
posterior pituitary
ACE
+
+
+
Arterioles
ANG II
Thirst
+
Adrenal
cortex
Vasoconstriction
osmolarity inhibits
Aldosterone
Peripheral
resistance
Distal
nephron
Distal
nephron
Na+
reabsorption
Blood
pressure
H2 O
and
reabsorption
Volume
H2 O
intake
Osmolarity
Figure 20-17 (5 of 6)
Volume and Osmolarity
Blood volume/
Blood pressure
DEHYDRATION
accompanied by
RENAL
MECHANISMS
RENIN-ANGIOTENSIN
SYSTEM
CARDIOVASCULAR
MECHANISMS
+
Carotid and aortic
baroreceptors
+
+
Granular
cells
CVCC
Flow at
macula densa
HYPOTHALAMIC
MECHANISMS Hypothalamic
osmoreceptors
Atrial volume
receptors; Carotid
and aortic
baroreceptors
+
Volume
conserved
Renin
Angiotensinogen
Parasympathetic
output
GFR
+
Osmolarity
Sympathetic
output
Hypothalamus
+
ANG I
Vasopressin
release from
posterior pituitary
ACE
+
Heart
+
+
+
Arterioles
ANG II
Thirst
+
Adrenal
cortex
Vasoconstriction
Rate
osmolarity inhibits
Force
Aldosterone
Peripheral
resistance
Distal
nephron
Distal
nephron
Na+
reabsorption
Cardiac
output
Blood
pressure
H2 O
and
reabsorption
Volume
H2 O
intake
Osmolarity
Figure 20-17 (6 of 6)
Acid-Base Balance
• Normal pH of plasma is 7.38–7.42
• H+ concentration is closely regulated
• Changes can alter tertiary structure of proteins
• Abnormal pH affects the nervous system
• Acidosis: neurons become less excitable and
CNS depression
• Alkalosis: hyperexcitable
• pH disturbances
• Associated with K+ disturbances
Acid-Base Balance
• Hydrogen ion and pH balance in the body
Fatty acids
Amino acids
H+
input
CO2 (+ H2O)
Lactic acid
Ketoacids
Plasma pH
7.38–7.42
Buffers:
• HCO3– in extracellular fluid
• Proteins, hemoglobin, phosphates in cells
• Phosphates, ammonia in urine
CO2 (+ H2O)
H+ output
H+
Figure 20-18
Acid and Base Input
• Acid
• Organic acids
• Diet and intermediates
• Under extraordinary conditions
• Metabolic organic acid production can increase
• Ketoacids
• Diabetes
• Production of CO2
• Acid production
• Base
• Few dietary sources of bases
pH Homeostasis
• Buffers
• Moderate changes in pH
• Combines with or releases H+
• Cellular proteins, phosphate ions, and hemoglobin
• Ventilation
• Rapid response
• 75% of disturbances
• Renal regulation
• Slowest of the three mechanisms
• Directly excreting or reabsorbing H+
• Indirectly by change in the rate at which HCO3– buffer is
reabsorbed or excreted
pH Disturbances
by Law of Mass Action
Negative feedback
Carotid and aortic
chemoreceptors
Plasma
PCO2
Central
chemoreceptors
Respiratory
control centers
in the
medulla
Action potentials in somatic
motor neurons
Negative feedback
• The reflex
pathway for
respiratory
compensation
of metabolic
acidosis
Plasma H+
( pH)
Muscles of ventilation
Rate and depth of breathing
Plasma H+
( pH)
by Law of Mass Action
Plasma
PCO2
Figure 20-19
pH Disturbances
• Overview of renal compensation for acidosis
Acidosis
pH = H+
Nephron
cells
HPO42–
filtered
Blood
CO2 + H2O
Carbonic Anhydrase
H+
secreted
H+ + HCO3–
H+
H2PO4–
Excreted
in urine
Amino acids +
NH4+
H+
HCO3–
reabsorbed
HCO3– buffer
added to
extracellular
fluid
Figure 20-20
Renal Compensation: Transporters
•
•
•
•
•
Apical Na+-H+ exchanger (NHE)
Basolateral Na+-HCO3– symport
H+-ATPase
H+-K+-ATPase
Na+-NH4+ antiport
Renal Compensation
• Proximal tubule H+ secretion and the
reabsorption of filtered HCO3–
Glomerulus
Bowman’s
capsule
Interstitial
fluid
Peritubular
capillary
1 Na+-H+ antiport
secretes H+.
Filtration
HCO3–
Proximal tubule cell
Na+
3 CO2 diffuses into cell
and combines with water
to form H+ and HCO3–.
1 Na+
Secreted H+
4
Na+
H+
+
4 H is secreted again
and excreted.
Na+
Filtered HCO3– + H+
2
+
2 H in filtrate combines
with filtered HCO3– to
form CO2.
HCO3–
Na+
HCO3–
5
CA
3
H2O + CO2
CO2 + H2O CA H+ + HCO3–
Reabsorbed
6 Glutamine
7
Secreted H+ and NH4+
will be excreted
NH4+
Na+
KG
5 HCO3– is reabsorbed.
6 Glutamine is metabolized
to ammonium ion and
HCO3–.
7 NH4+ is secreted and
excreted.
HCO3–
HCO3–
Na+
Na+
8
8 HCO3– is reabsorbed.
Figure 20-21
Intercalated Cells
• Type A
intercalated
cells function in
acidosis
Figure 20-22a
Intercalated Cells
• Type B
intercalated
cells function in
alkalosis
Figure 20-22b
Acid-Base Balance
Table 20-2
Summary
• Fluid and electrolyte homeostasis
• Water balance
• Vasopressin, aquaporin, osmoreceptors,
countercurrent multiplier, and vasa recta
• Sodium balance
• Aldosterone, principal cells, ANG I and II, renin,
angiotensinogen, ACE, and ANP
• Potassium balance
• Hyperkalemia and hypokalemia
Summary
• Behavioral mechanisms
• Integrated control of volume and osmolarity
• Acid-base balance
• Buffers, ventilation, and kidney
• Acidosis and alkalosis
• Intercalated cells

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