Nucleus cytoplasm extracellular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7%...

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nucleus cytoplasm extracell ular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7% 26% 67%

Transcript of Nucleus cytoplasm extracellular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7%...

nucleus

cytoplasm

extracellular fluid

waterNa+K+Cl-sugarsproteins

plasma

intracellular fluid

7%

26%

67%

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)

As this column rises higher, it will exert increasing pressure. At some point that hydrostatic pressure will reach an equilibrium, at which pointno more net water will move across thesemi-permeable membrane.

This pressure is the ‘osmotic pressure’of the starting solution on the right.

Osmotic flux of water: --which way will the water move?-- Why is there net water flux tothe right?

isosmotic

Solutes are dissolved particles in solution (any type)

(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

Hyposmotic (lower osmotic pressure)

Hyperosmotic (higher osmotic pressure)

osmotic pressure: the pressure of water to enter, given the solute concentration

Osmosis: movement of water from anArea with lower osmotic pressure to Higher osmotic pressure

Osmolarity= concentration of solutes in a solution

Osmolarity vs. Molarity:

150 mMol sucrose= 150 mOsm sucrose

150 mMol NaCl = 300 mOsm NaCl

Osmotic pressures are generally described in osmolar units:

Definitions

• Solute:• Solvent:• Osmosis:• Osmotic Pressure:• Osmolarity:• Hyperosmotic:• Hypoosmotic:

Dissolved particles in a solution

movement of water from an area with lower osmotic pressure to higher osmotic pressure the pressure of water to enter,

given the solute concentration

Concentration of solutes in a solution

Higher osmotic pressure

Lower osmotic pressure

What the particles are dissolved in

The Mammalian Kidney

glomerulus

Bowman’scapsule

Proximal tubule

Loop of Henle

Distal tubule

Collectingduct

To bladderExtracellular Na+ conc.

Passive movement of water

H2O

Active movement of Na+

Na+

HIGH

LOW

What it actually looks like

Bowman’s capsule

Distal tubuleProximal tubule

Loop of Henle

glomerulus

Collecting duct

Osmotic ImbalanceHypovolemia

Baroreceptors in arteries of the heart

Causing an increase in secretion and release

of VP

VP2 major effects:1. Vasoconstriction2. Water retention in kidney

Collecting Duct Cell

glomerulus

Bowman’scapsule

Proximal tubule

Loop of Henle

Distal tubule

Collectingduct

To bladder

Passive movement of water

H2

O

The water pore is a protein called:aquaporin 2 (AQP2)

Collecting Duct:

n n

filtrate

to bladder

Basal side of cellapical side

of cell

Lower Na+

Higher Na+

Extracellular space

Collecting Duct:n n

to bladder

Lower Na+

Higher Na+

No Vasopressin:

basal aquaporins

Aquaporin 2

H2O

H2O

H2O

Add Vasopressin:

Collecting Duct:n n

to bladder

Lower Na+

Higher Na+

basal aquaporins

Aquaporin 2

H2O

H2O

H2O

Add Vasopressin:

Collecting Duct Cross-Section

Cells labeled with fluorescent antibodies made to the water channel

n n

Collecting Duct:

Collecting Duct:

Stain for aquaporin 2 (no vasopressin):

Collecting Duct:

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. Vasoconstriction2. Water retention in kidney:

Collecting Duct Cell

V2 receptor: localized to the kidney

VP

Gq

PLC

IP3

DAG

Smooth muscle cellIn arteries/capillaries

V1a receptor: localized to vascular smooth muscle cells

V1a receptorV2 receptor

Hypovolemia

Control of Aldosterone Secretion

ReninSecreted in response to low blood pressure

Cells in the capillary walls

ANGIOTENSIN I

ANGIOTENSIN II

angiotensin converting enzyme(ACE: secreted by the lungs)

IN THE BLOOD

ANGIOTENSINOGEN Made in the liver

aldosterone

Adrenal gland(cortex)

glomerulus

Bowman’scapsule

Proximal tubule

Loop of Henle

Distal tubule

Collectingduct

To bladderExtracellular Na+ conc.

Active movement of Na+

Na+

ALDOSTERONE:

Increases uptake of sodium from filtrate -Increases sodium in the blood -Decreases sodium in urine

Aldosterone and Angiotensin II productionIN THE BLOOD

ANGIOTENSINOGEN

ANGIOTENSIN I

ANGIOTENSIN II

angiotensin converting enzyme(ACE: secreted by the lungs)

Made in the liver

aldosteroneIncreases Na+ absorbtion in the kidney

Reninfrom glomerulus

Induce release of VP

Cause vasoconstriction

Stimulate drinking

REVIEW: hypovolemia

• 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

A Decrease in Blood Pressure:

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

VP

2 major effects:1. Vasoconstriction2. Water retention in kidney

Neural cells in hypothalamus containing osmoreceptors

Vasopressin and Osmolality

Angiotensin and Aldosterone?

Cells in the capillary walls

These cells are also sensitive to osmolality

-under low osmolality they secrete renin

-under high osmolality the shut down renin secretion

Under conditions of high osmolalityIN THE BLOOD

ANGIOTENSINOGEN

LESS ANGIOTENSIN I

LESS ANGIOTENSIN II

angiotensin converting enzyme(ACE: secreted by the lungs)

Made in the liver

LESS aldosteroneDecreases Na+ absorbtion in the kidney

LESS Renin from glomerulus

less VP

less vasoconstriction

less drinking

Osmotic Imbalance Review

• 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

High blood osmolality causes:

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

VP

Vasopressin is synthesized and secreted normally

Collecting Duct Cell

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

A B C

Hypothalamus

Posterior Pituitary