Kidney Function Iv Regulation Of Osmolarity And Blood Volume

Front 1

What is normal osmolarity?

Back 1

290 mmos/l

Front 2

What happens if there is water depreivation, solute ingestion,diarrhoea etc?

Back 2

increased ECFosmolarity

Front 3

What does increased ECF osmolarity lead to?

Back 3

Detected by OSMORECEPTORS:

supraoptic ¶ventricularNuclei

lateralpreopticarea

Front 4

What do the supraoptic and paraventricular Nuclei cause to happen?

Back 4

ADH releasefrom posteriorpituitary

Front 5

What does the ADH do?

Back 5

CD made waterpermeable

Front 6

What does increased water permeability of the CD lead to?

Back 6

WATER RETENTION by Kidney returning plasma osmolarity back to normal

Front 7

What does the lateral preoptic area stimulate?

Back 7

thirst ---> drink water ----> plasma osmolarity returned to normal

Front 8

Does the regulation of plasma osmolarity only work in this direction?

Back 8

Regulation works in bothdirections

Front 9

What does the tight control of ECF osmolarity mean for the regulation of ECF volume?

Back 9

Since the osmolarity (i.e. water concentration) ofECF is tightly controlled,

the volume of the ECF is determined by the totalquantity of solute (mainly NaCl),

so regulation of ECF volume is all about sodiumbalance.

Front 10

What does the dietary salt intake range between?

Back 10

Dietary salt (NaCl) intake varies 0.05-25g/day.Average 2.3g/day

Front 11

What does the total amount of Na in ECF dictate?

Back 11

Volume Regulation .. The total amount ofSodium in ECF dictates volume of ECF

Front 12

What is plasma volume an important determinant in?

Back 12

PLASMA VOLUME important determinant of blood pressure in veins, cardiacchambers and arteries.

So low total body sodium leads to low plasma volumewhich leads to low cardiovascular pressures

Front 13

What are the key points in the control of osmolarity in the ECF?

Back 13

• Body directly controls osmolarity and volume of ECF invascular system.

• This affects the osmolarity and volume of the othercompartments.

• Normally osmolarity is maintained at expense of volume.

• Osmoreceptors control H2O

i) renal excretion by altering ADH release.

ii) intake by altering thirst.

Front 14

What is Na+ content largely regulated by?

Back 14

Na+ content is largely regulated by kidney by controlling

i) GFR

ii) Sodium Reabsorption

Front 15

What is there little evidence for?

Back 15

Little evidence for regulatory “Na+ appetite” in humans

Front 16

What is the extrinsic control of GFR?

Back 16

Activation of sympathetic nervoussystem (baroreceptor response).

Front 17

How does the sympathetic do to decrease GFR?

Back 17

*Vasoconstricts afferent arteriole - DECREASES GFR.*Reduces surface area of filtration barrier viamesangial cells - DECREASES GFR.

Front 18

What will reduction in GFR do?

Back 18

Reduction in GFR will conserve sodium andwater

Front 19

What is intrinsic Control of GFR(protects renal capillaries and maintains a healthy GFR)?

Back 19

Autoregulation (within kidney)

Front 20

What can autoregulation do?

Back 20

Can control afferent arteriole constriction

Front 21

What mechanisms does autoregulation include?

Back 21

Tubuloglomerular feedback

Myogenic feedback

Front 22

Within which arterial pressures will Renal Blood flow and GFR remain constant?

Back 22

Renal blood flow (RBF) andGFR remain constant forarterial pressures between 90-200 mmHg

Front 23

What do afferent arterioles do when BP is raised or lowered?

Back 23

Afferent arterioles constrictwhen BP is raised and dilatewhen BP is lowered, thusmaintaining constant capillarypressure and glomerular bloodflow

Front 24

What controls Na reabsorption?

Back 24

Multiple regulatory pathways controllingsodium reabsorption

Front 25

What are the sensors in the regulatory pathways?

Back 25

Tubular fluid NaCl concentration receptors within macula densa.

Pressure receptors in central arterial tree.Pressure receptors in renal afferent arterioles (intrarenal baroreceptors).

Volume receptors in cardiac atria and intrathoracic veins

Front 26

What are the effector pathways?

Back 26

Renal sympathetic nerves (stimulate renin release)

Renin/angiotensin II/aldosterone (stimulate Na+ reabsorption)

Atrial Natriuretic Peptide (causes natriuresis, inhibits Na+ reabsorption)

Direct pressure effect on kidneyDopamine (causes natriuresis, inhibits Na + reabsorption)

Front 27

What does activation of the sympathetic nerves do?

Back 27

•Vasoconstricts afferent arteriole - decreases GFR.

• Reduces surface area of filtration barrier viamesangial cells - decreases GFR.

• Stimulates renin release.

Front 28

Where do the sympathetic nerves of granular cells receive signals from?

Back 28

Sympathetic nerves of granular cells receive signals frombaroreceptors in central arterial tree via cardiovascular centre

Front 29

What does the juxtaglomerular apparatus consist of?

Back 29

the juxtaglomerular apparatus(JGA) includes juxtaglomerular cells and macula densa.

Front 30

What type of control is tubuloglomerular feedback?

Back 30

Tubuloglomerular feedback (Intrinsic control)

Front 31

What is the mechanism of tubuloglomerular feedback?

Back 31

Increased NaCl to the macula densa will lead to an increased formation rate of adenosine (ADO)which through A1 receptors causes an increase in calciumthat contracts the afferent arteriole and inhibits renin release.

Front 32

What is the sensor in this pathway?

Back 32

Macula densa (sensor)

Front 33

What is the Renin (effector pathway)?

Back 33

Renin may be released by:

decreased sodium delivery to Macula Densa

decreased wall tension in the afferent arteriole(e.g. a drop in mean or pulse pressure)

sympathetic activity (e.g. baroreceptor response to low BP)

i.e. can be caused by Low Blood Volume(Hypovolemia)

Front 34

How is angiotensinogen converted to Angiotensin I?

Back 34

Renin

Plasma angiotensinogen ------> Angiotensin I (10 - peptide)

Front 35

How is Angiotensin I converted to Angiotensin II?

Back 35

ACE

Angiotensin I (10 - peptide) ------> Angiotensin II (8 - peptide)

Front 36

What does angiotensin II do?

Back 36

StimulatesProximal TubuleNa+reabsorption

StimulatesADH Release

Causes AldosteroneSecretion

CausesThirst

Vasoconstrictssmall arterioles

Front 37

How does Angiotensin II stimulate Proximal Tubule Na+ reabsorption?

Back 37

Angiotensin IIStimulatesProximal TubuleNa+reabsorption bybinding to AT1receptors

AT1 = Angiotensin II Type 1receptor

Front 38

Where is aldosterone released from?

Back 38

Aldosterone released from adrenal cortex

Front 39

What does aldosterone cause?

Back 39

Increased Sodium Reabsorption in DCT and CD

Front 40

What does Increased Sodium Reabsorption in DCT and CD lead to ?

Back 40

Osmoregulation -----> Expansion of ECF

Front 41

What does the expansion of the ECF lead to?

Back 41

Restoration ofVolume

Front 42

As well as increasing Na+ Reabsorption in the DCT and CD, where else does Aldosterone act?

Back 42

Increases Na+reabsorption in DCT and CD

as well as from:

– sweat glands

– salivary glands

Increases Na+ absorption from gut

Front 43

Where is Aldosterone secreted from and why is this?

Back 43

Secreted by zona glomerulosa in adrenal cortex.Due to

(a) Angiotensin II

(b) increased plasma K+ concentration

Front 44

Why is the action of Aldosterone slow?

Back 44

Aldosterone, like other steroids, binds tonuclear receptors and stimulates proteinsynthesis, so its actions are slow, comparedwith ADH

Front 45

Where is the main area of action of Aldosterone?

Back 45

Its main action is on the principalcells of the collecting duct where it stimulatesNa+ reabsorption by stimulating production ofNa+:K+ pumps and epithelial Na+ channels(ENaC). Water follows Na+.

Front 46

When aldosterone secretion is stimulated by (b) increased plasma K+ concentration, what is it's effect?

Back 46

It also acts on the principal cells of thecollecting duct to stimulate K+ secretion.

Front 47

What channels does aldosterone act on?

Back 47

(Epithelial sodium channel; ENaC)

(Renal Outer Medullary K+ channel; ROMK)

(Ca2+ activated big-conductance K+ channel; BK)

Front 48

What is an example of a volume sensor?

Back 48

Volume sensor.... The heart

Front 49

What are released when the heart is stretched?

Back 49

Natriuretic Peptides (NP) released when the heart stretched(due to blood volume)

Front 50

Where are the different types secreted from?

Back 50

A type secreted from atrial myocardium (ANP).

B type secreted from ventricular myocardium (BNP).

Front 51

What do natiuretics do?

Back 51

acts on collecting ductcells to inhibit Na+ entry throughepithelial sodium channels (ENaC),inhibits renin release andaldosterone production. Synergismwith dopamine to inhibit Na + -K+ATPase activity in proximal tubule.

Front 52

What does a Diuretic do?

Back 52

Diuretic: inhibits ADH release.

Front 53

What are the hypotensive effects of ANP and BNP?

Back 53

Hypotensive effects: decreasesblood pressure by vasodilation;increases GFR by dilating afferentarterioles

Front 54

What channels do ANP and BNP act on?

Back 54

(Epithelial sodium channel; ENaC)

(Renal Outer Medullary K+ channel; ROMK)(Ca2+activated big-conductance K+ channel; BK)

Front 55

How could ANP enhance dopamine tubular transport?

Back 55

ANP could enhance dopamine tubulartransport in proximal tubule cells, by stimulation of organic cationic transporters