osmoregulation

advertisement
intracellular fluid
67%
plasma
extracellular
fluid
26%
7%
water
Na+
K+
Clsugars
proteins
nucleus
cytoplasm
Definitions
•
•
•
•
•
•
•
Solute
Solvent
Osmosis
Osmotic Pressure
Osmolarity
Hyperosmotic
Hypoosmotic
Solutes are dissolved particles in
solution (any type)
• Osmotic pressure depends on the number of solutes/unit
volume (rather than chemical nature of solutes)
Osmotic flux of water:
--which way will the water move?
-- Why is there net water flux tothe right?
As this column rises higher, it will
exert increasing pressure. At some
point that hydrostatic pressure will
reach an equilibrium, at which point
no more net water will move across the
semi-permeable membrane.
This pressure is the ‘osmotic pressure’
of the starting solution on the right.
Solutes are dissolved particles in
solution (any type)
isosmotic
(osmotic pressure is equal)
Solutes are dissolved particles in
solution (any type)
hypersmotic
(higher osmotic pressure)
hyposmotic
(lower osmotic pressure)
Water always moves from an area of low osmotic
pressure to an area of high osmotic pressure
osmotic pressure: the pressure of
water to enter, given the solute
concentration
Hyposmotic (lower
osmotic pressure)
Hyperosmotic (higher
osmotic pressure)
Osmosis: movement of water from an
Area with lower osmotic pressure to
Higher osmotic pressure
Osmotic pressures are generally
described in osmolar units:
Osmolarity
= concentration of solutes in a solution
Osmolarity vs. Molarity:
150 mMol sucrose = 150 mOsm sucrose
150 mMol NaCl
= 300 mOsm NaCl
Definitions
•
•
•
•
•
•
•
Solute: Dissolved particles in a solution
Solvent: What the particles are dissolved in
movement of water from an area with lower
Osmosis: osmotic pressure to higher osmotic pressure
Osmotic Pressure: the pressure of water to enter, given
the solute concentration
Osmolarity: Concentration of solutes in a solution
Hyperosmotic: Higher osmotic pressure
Hypoosmotic: Lower osmotic pressure
The Mammalian Kidney
Active movement of Na+
Passive movement of water
Distal tubule
Proximal tubule
LOW
Collecting
duct
Bowman’s
capsule
Na+
glomerulus
H2O
To bladder
Extracellular
Na+ conc.
Loop of Henle
HIGH
What it actually looks like
Distal tubule
Proximal tubule
Bowman’s capsule
glomerulus
Collecting duct
Loop of Henle
Hypovolemia
Osmotic Imbalance
Causing an increase in
secretion and release
of VP
Baroreceptors
in arteries of the heart
VP
2 major effects:
1. Vasoconstriction
2. Water retention in kidney
Passive movement of water
Proximal tubule
Distal tubule
Collecting
duct
Bowman’s
capsule
glomerulus
H2
O
To bladder
Loop of Henle
The water pore is a protein called:
aquaporin 2 (AQP2)
Collecting Duct Cell
n
Collecting Duct:
n
filtrate
Extracellular space
Lower Na+
Basal side of cell
apical side
of cell
Higher Na+
to bladder
Collecting Duct:
n
n
H2O
Lower Na+
basal aquaporins
H2O
Aquaporin 2
No Vasopressin:
Add Vasopressin:
H2O
Higher Na+
to bladder
Collecting Duct:
n
n
H2O
Lower Na+
basal aquaporins
H2O
Aquaporin 2
Add Vasopressin:
H2O
Higher Na+
to bladder
Collecting Duct Cross-Section
Cells labeled with fluorescent antibodies made to the water channel
n
Collecting Duct:
n
Collecting Duct:
Collecting Duct:
Stain for aquaporin 2 (no vasopressin):
Collecting Duct:
Stain for aquaporin 2 (no vasopressin):
Add Vasopressin:
Collecting Duct:
Stain for aquaporin 2:
Add Vasopressin:
Collecting Duct:
2 major effects of vasopressin:
1. Vasoconstriction
2. Water retention in kidney:
V1a receptor
V2 receptor
Smooth muscle cell
In arteries/capillaries
Collecting Duct Cell
VP
DAG
PLC
Gq
IP3
V1a receptor: localized
to vascular smooth
muscle cells
V2 receptor: localized to the kidney
Hypovolemia
Control of Aldosterone Secretion
IN THE BLOOD
Renin
ANGIOTENSINOGEN
Made in the liver
Secreted in response
to low blood pressure
ANGIOTENSIN I
angiotensin converting enzyme
(ACE: secreted by the lungs)
ANGIOTENSIN II
Adrenal gland
(cortex)
aldosterone
Cells in the capillary walls
ALDOSTERONE:
Increases uptake of sodium from filtrate
-Increases sodium in the blood
-Decreases sodium in urine
Active movement of Na+
Distal tubule
Proximal tubule
Collecting
duct
Bowman’s
capsule
Na+
glomerulus
Extracellu
lar Na+
conc.
To bladder
Loop of Henle
Aldosterone and Angiotensin II production
IN THE BLOOD
Made in the liver
ANGIOTENSINOGEN
Renin
from glomerulus
ANGIOTENSIN I
angiotensin converting enzyme
(ACE: secreted by the lungs)
Stimulate drinking
ANGIOTENSIN II
Cause vasoconstriction
Induce release of VP
aldosterone
Increases Na+ absorbtion in the kidney
REVIEW: hypovolemia
A Decrease in Blood Pressure:
• Heart baroreceptors cause
posterior pituitary to secrete VP
– VP increases vasoconstriction
– VP increases water pores in the
collecting duct, increasing water
absorbtion from filtrate
• Cells in glomerulus secrete renin
–  angiotensin II
•
•
•
•
Increases aldosterone
Increases vasoconstriction
Increases VP
Stimulates drinking
–  aldosterone
• Increase sodium retention
What about an increase in blood
pressure?
• Baroreceptors in heart stop sending
releasing signals to SON and PVN
• Glomerulosa cells produce less renin
• Under conditions of excessively high blood
pressure:
– The atria of the heart secrete Atrial Natriuretic
Peptide (ANP)
– ANP:
• Shuts down secretion of VP, renin, and ALDO
• Increases sodium excretion in the urine
• Increases diuresis (water loss in urine)
Osmotic Imbalance
Osmoreceptors:
-Present in cells in the
hypothalamus
-when dehydrated,
cause secretion of VP
from PVN and SON
Neural cells in hypothalamus
containing osmoreceptors
VP
2 major effects:
1. Vasoconstriction
2. Water retention in kidney
Vasopressin and Osmolality
Angiotensin and Aldosterone?
These cells are also sensitive to
osmolality
-under low osmolality they secrete
renin
-under high osmolality the shut
down renin secretion
Cells in the capillary walls
Under conditions of high osmolality
IN THE BLOOD
Made in the liver
ANGIOTENSINOGEN
LESS Renin from glomerulus
LESS ANGIOTENSIN I
angiotensin converting enzyme
(ACE: secreted by the lungs)
less drinking
LESS ANGIOTENSIN II
less vasoconstriction
less VP
LESS aldosterone
Decreases Na+ absorbtion in the kidney
Osmotic Imbalance Review
High blood osmolality causes:
• Osmoreceptors in the brain to
signal SON and PVN nuclei to
increase VP secretion
– VP increases water retention in the
kidney
• Glomerular cells decrease
secretion of Renin
– Decrease Aldosterone secretion
– Decrease Angiotensin II levels
Pathophysiology of Osmoregulatory
processes
• Adipsic hypernatremia
– Dipsia is thirst, hypernatremia is high salt load
– These patients do not have osmoreceptors in the brain, so they don’t
respond to hyperosmolality of the blood
No osmoreceptors in the brain
–No osmoreceptors, no VP secretion
in response to cellular dehydration
–They need water, but they aren’t
thirsty
–They do, however, have functional
baroreceptors, and respond normally
to changes in blood pressure
Pathophysiology of Osmoregulatory
processes
• Adipsic hypernatremia
– Dipsia is thirst, hypernatremia is high salt load
– These patients do not have osmoreceptors in the brain, so they don’t
respond to hyperosmolality of the blood
– No osmoreceptors, no VP secretion in response to cellular
dehydration
– They need water, but they aren’t thirsty
• Diabetes Insipidus
– Two types:
• Neurogenic DI:
• Nephrogenic DI:
Neurogenic Diabetes Insipidus
VP is made but not
transported
VP
1. no VP is secreted
2. Very little water is retained in the collecting duct
Treatment with VP
can alleviate the
problem
Nephrogenic Diabetes Insipidus
Collecting Duct Cell
Vasopressin is
synthesized and
secreted normally
VP
But there is a defect in the cellular mechanism that responds to VP
Pathophysiology of Osmoregulatory
processes
• Adipsic hypernatremia
– Dipsia is thirst, hypernatremia is high salt load
– These patients do not have osmoreceptors in the brain, so they don’t
respond to hyperosmolality of the blood
– No osmoreceptors, no VP secretion in response to cellular
dehydration
– They need water, but they aren’t thirsty
• Diabetes Insipidus
– Two types:
• Neurogenic DI: Problem with VP secretion
• Nephrogenic DI: Problem with VP receptors in collecting duct
• Malignant hypertension
Pathophysiology of Osmoregulatory
processes
• Adipsic hypernatremia
– Dipsia is thirst, hypernatremia is high salt load
– These patients do not have osmoreceptors in the brain, so they don’t
respond to hyperosmolality of the blood
– No osmoreceptors, no VP secretion in response to cellular
dehydration
– They need water, but they aren’t thirsty
• Diabetes Insipidus
– Two types:
• Neurogenic DI: Problem with VP secretion
• Nephrogenic DI: Problem with VP receptors in collecting duct
• Malignant hypertension
– Causes a sudden and severe rise in blood pressure
– Can lead to blindness, seizure, chest pain, heart failure
Hypothalamus
Posterior
Pituitary
A
B
C
Download