Biology - unit 6.4 homeostatis - 6.4.1 principles of homeostatsi and negative feedback, 6.4.2 control of blood glucose conc , 6.4.3 control of blood water potential

What is homeostasis?

maintenance of a constant internal environment with restriced limitis [optimum] . This involves physiological control systems

describe hormones - produced where? secreted into? carried in the what in the blood? act on? whats special about these things they act on? effective in high/low concs? long or short lasting effects?

- produced in glands and secreted into bloodsteam. carried in the plasma and act on target cells, which the target cells often have specific receptors on their cellsurface that are complementary to a specific hormone. they are effective in low concentrations with widespread and long lasting effects

why does homeostasis matter to enzymes? proteins with change in temp, change in ph

proteins - including enzyes[eg membrane-carrier proteins , or antibodies] are effected by temp and ph.

-change in temp = a change in tertiary structure (ionic, disulfide hydrogen bond..) = change in function

- change in ph = change in tertiary structure = change in function

why does homeostasis matter to water potential? for more and less neg water potential

- more neg water pot in blood [hypertonic = high conc of blood glucose low water ]will cause water to move out of cells by osmosis (into the blood) - therefore these surrounding cells will become flaccid - die, shrivel

- less neg water pot [hypotonic]will cause water to move out of the blood into the surrounding cells by osmosis - and therefore they will burst and do cell lysis

blood shouls be isotinic - no net osmosis inot or out of the cell

describe the homeostatic control systems - this that cyclical graoh think with the gre bubbles at bot of page - 4 steps

1. receptor -detects a stimulus

2. control centre - coordinates information/response

3. effector - brings about a response that returns conditions back to optimum - negative feedback - e.g muscles that contract, glands that release hormones

4. variable - a factor in the body that can be modified by effector ??// - was meantt to wrte on this one?

whats positive feedback?

deviation from 'normal' causes changes that result in an even greater deviation from the 'norm' [optimum/restricted limits]

e.g opening of v gated na+ channels and influx of na+ during an action potential

BASO THE CHANGE CAUSES AN EVEN BIGGER CHANGE

Whats negative feedback?

the change produced by the control system to restore a variable back to optimum, opposing the original deviation

e.g blood glucose control, control of blood water potential, thermoregulation

BASO LIKE CORRECTING IT and restoring normal function

what kicks the homeostasis cycle into gear. the response of the effector negates the stimulus and restores normal function

describe the effects of homeostasis with negatuve feedback in thermoregulation in mammmals if its too hot [ body temp above 37.5] - 2 processes that happen

1. vasodilation [ i think just like expanding,relaxing] of arterioles = more blood flows into capilaries near skin surface = more radiation of heat

2. you sweat more = increased evaporisation of water - therefore loss of heat from body

describe the effects of homeostasis with negatuve feedback in thermoregulation in mammmals if its too cold [ body temp below 37.5] - 2 processes that happen

1. vasoconstriction of arterioles = less blood flows ingo capilaries near surface of skin = les radiation of heat

2. shivering = rapid muscle contraction = increased respiration = releases lots of heat as is an exothermic reaction

describe the steps sipmly in negative feeback system?

-stimulus - change detected - receptor - impluse sent via afferent pathway - control centre - output sent via efferent pathway - effector - response opposes change

whats glucose needed for?

respiration and to mmake ATP

What does glucose do when its in the blood?

lower [make more neg] the water potential - causing water to move out of the cells by osmosis

where are the alpha cells found, and what do they produce?

in the islets of Langerhans [in pancreas] and produce GLUCAGON

where are the beta cells found, and what do they produce?

in the islets of langerhans and they priduce INSULIN

How do alpha and beta cells act?

antagonistically - bring about the opposite action - only 1 works at a t e - so opposite things

whats the song for low blood sugar?

"when the glucose is gone, we need our glucagon"

what acc are the iskets of langerhans?

clusters of alpha and beta cells

descrobe the process of if you have low blood sugar [the seneca v good for this btw]

1. low blood sugar = promotes glucagon release

2. this happens where the glucagon is produced in the alpha cells in the islets of langerhans[in pancreas], and

3. the glucagon stiulates glycogen breakdown

4. glycogen is broken down into glucose IN LIVER

5. this glucose raises the blood sugar

descrobe the process of if you have high blood sugar [the seneca v good for this btw]

1. high blood sugar promotes insulin release

2. this happens where the beta cells produce the insulin in the islets of langerhans [in pacnreas]

3. the insulin situmulate BOTH glucose uptake from blood [ taking it out the blood] eg through tissue cells and also through stiulating glycogen formation where glucose is broken down into glycogen in the LIVER

4. these both lowers the blood sugar

so alpha cells?

alpha = glucagon = for low glucose concs - makes more glucose

beta cells?

beta = inuslin = when blood glucose conc too high - turns glucse into glycogen and stores it

what organ are insulin and glucagon produced in?

pancreas

where is the location that hormones have most of their effects?

LIVER

what are the 3 main functions that the liver carries out?

1. glycogenesis

2. glycogenolysis

3. gluconeogenesis

whats glycogenesis? when blood glucose is too? what hormone involved?

conversion of glucose to glycogen by liver

when blood glucose = too high

insulin - [insulin always high on glucose]

THINK nesis - because you converting the small glucose with tiny knees into glycogen

whats glycogenolysis? when blood glucose is too? what hormone involved?

breakdown of glycogen to glucose by liver

when blood glucose = too low

glucagon + adrenaline

think lysis - because YOUR BREAKING DOWN glycogen to glucose - Break down TH EBIG FATTY GLYCOGEN

whats gluconeogenesis? when blood glucose is too? what hormone involved?

production of glucose from non-carbohydrate sources [eg glycerol + amino acids}

when blood glucose = too low

glucagon

think NEW glucose - cause neo

describe secondary messanger vodel thing simply - and the opposite m scheme version

Low glucose = detected by alpha cells in isletels of langerhan in pancreas = secrete glucagon and adrenaline which bind to the target cell = muscle cell = stimulates adenylate cyclase - which converts ATP into cAmP - which stivulates Protein kinase A - which dtimulates glucgoneogenis and glycogenolysis

1. Less/no ATP is converted to cyclic AMP/cAMP;

2. Less/no kinase is activated;

3. Less/no glycogen is converted to glucose

wheres adrenaline made?

adrenal glands

whats the overall purpose of insulin?

to decrease blood glucose concentration

where is insulin released by/from?

beta cell in the islets of Langerhans - think insulin is kitkat and you break kitkats so its beta cells

when they detect high blood glucose

how does insulin bring about its 3 changes [ like dont describe the 3 chnages - but the first step]

its released by beta cells in the isles of Langerhans, and then binds to GLYCOPROTEIN RECEPTORS on the CSM, brinign about 3 changes

how does insulin lower blood glucose conc in blood change 1? IBR

1. !insulin binds to receptors! on the CSM, causes a tertiary structure change of glucose channel proteins in the membrane

= glucose channels open

= glucose moves into cells [out of blood] by facilitated diffusion

how does insulin lower blood glucose conc in blood change 2? ICVF

! insulin causes vesicles to fuse!

1. insulin causes vesicles [with glucose channel proteins in the membrane] to fuse with the CSM

2. - therefore more glucose channel proteins emmbedded in the CSM [ the channel proteins are left behind/stuck in the ebrane]

3. = increased PEREABLITY of the cell to glucose = more uptake of glucose by facilitated diffusion [ baso ore channels in CSM - so ore glucose can difuse in]

how does insulin lower blood glucose conc in blood change 3? IAE

! Insulin activates enzymes!

1. insulin activates enzymes that convert glucose to glycogen within the cell = GLYCOGENESIS

exam q - how does a lack of insulin affect reabsorption of glucoe in the kidneys of a person who does not secrete insulin?

1. high conc of glucose in blood

2. high conc in tubule/filtate

3. reabsorbed by faciliated diffusion/active transport

4. requires proetins/carriers

5. these are workiing at max ate

6. not all glucose is reabsorved/some lost in urine

HOW TO REMEMBER THE GLYCOGENESIS, GLUCONEOGENESIS, GLYCOGENOLYSIS ?

1. genesis = to make - anf glyco=glycogen so = make glycogen [so breaking down glucose into glycogen]

2. gluco = glucose, neo=new, genesis= make so = make new glucose - and to make new ones it has to be from non-carbohydrate sources - glycerol and amino acids

3. glyco = glycogen , lysis = break down - so = break down glycogen into glucose

how do the 3 diff processes of insulin lowering glucose blood conc acc reduced gluocse blood conc? 4 ways

1. increased glucose absortion into cells [liver and muscles]

2. increased rate of glycogenesis [mmaking glycogen - so not glucose, and using up glucose}

3. increased rate of respiration = uses more glucose = increased uptake into cells [maintains conc gradient]

4. increased rate if cinversion of glucose to fat

and so all of these decrease the blood glucose conc which = beta cells then stop needing to produce insulin = negative feedback

whats the overall purpose of glucagon?

to increase blood glucose concentration - "when the glucose is gone you need glucagon" and adrenaline works wth glucsagon - and insulin is just the opposite

where is glucagon released by/from?

alpha cells in the islets of Langerhans[pancreas] when they detect low blood glucose

alpha = low

what are the 3 ways glucagon works by?

1. attaching to specific receptor proetins on the cell mmebrane of LIVER CELLS[liver = targer cells/organ]

2. activating enzymes that convert glycogen to glucose [ glycogenolysis}

3. activating enzymes that are involved in converting AAs + glycerol [non-carbohydrate sources] into glucose = gluconeogenesis

and then the glucose from these 2 sources is released into the bloodstream via facilitated diffusion - so blood gluc conc levels back to normal and alpha cells detect this and stop making glucagon - negative feedback

how does inhibitng adenylate cyclase help to lower the blood glucose concentration?

- less ATP is converted to cyclicAMP/cAMP

- less kinase is activated

- les glycogen is converted to glucose [less gylcogenolysis]

What's type 1 diabetes?

a disorder in which the body cant produce insulin - due to damage to the beta cells and its often autoimune [immmune system attacking itself]

- its charactersised by uncontrolled high blood glucose levels

whats type 2 diabetes?

the body stops responding to insulin

- normmally due to glycoprotein receptors on the CSM of body cells being lost or unresponsive

a risk factor is obesity

what is a key differecne between diabetes 1 and 2?

1 = insulin dependent - as in you need like insulin injections to help you - like with ur high glucose levels

2 = insulin independent - like guess you just dont get injections, cause they wouldnt help, cause body dont respond to it

describe the example of the secondary messenger model - adrenaline and glucagon action - this that diagra with the cute looking floating robot thing - diagram quite big over half of the pagedescribe the example of the secondary messenger model - adrenaline and glucagon action - this that diagra with the cute looking floating robot thing - diagram quite big over half of the page

1. adrenaline binds to receptor protein on the liver cells CSM

2. binding of adrenaline causes protein to change shape (tertiary structure) on the inside of the membrane

3. this change in shape actviates an enzyme called Adenyl cyclase - which converts ATP to cyclic AMP = cAMP

4. cAMP binds to the protein kinase, changing its shape and so activating it

5. activated protein kinase catalyses the conversion of glycogen to glucose [glycogenolysis]

and then the glucose moves out of liver into bloodstream via facilitated diffusion

how are diabetes 1 and 2 treated?

1 = insulin injections, alongside mmanaging carbohyrdate intake and exercising carefully

2 = a carbohydrate controlled diet and an exercise regime

how to remmember different dibetes?

1 = skinny, cause you cant produce insulin and insulin = kitkat, so you baso cant eat food, so have to get insulin/kitkat inkections

2 = 2 people cant respond to one kitkat/insulin

osmoregulation is?

the control of water potential of the blood

what does renal refer to?

kidney

what is the cortex [ in the structure of the kidney] and what does it contain?

the lighter coloured outer layer of the kidney

contains:

- bowmans capsule

- PCT [proximal convoluted tubule] and DCT[distal convoluted tubule]

- blood vessels

what is the medulla [ in the structure of the kidney] and what does it contain?

the darker coloured inner layer of the kidney

- loop of Henle

- collectin ducts

- blood vessels

for the calibration curve pratical whTS THE mark sche em for that stupid 4 mmarjer - you know th e one - like how would u produces a calibration curve for [creatine]?

1. Use (distilled) water and creatinine solution to produce dilutions (series);

Accept description of dilutions (series).

2. [ +3} Addition of (creatinine-)detecting solution (to each solution);

The addition of a known/specific volume of (creatinine-)detecting solution = 2 marks.

4. Record absorbance/transmission of solution/s using a colorimeter;

Reject calorimeter. Ignore details provided on 'blank'.

Accept description of absorbance or transmission.

5. Plot dilution/concentration of (creatinine) solution against absorbance/transmission;

Accept absorption for 'absorbance'.

Accept description of absorbance or transmission.

4 max

and whats the follow up 2 marker asnwer for that horrible calibration 4 marker - th eone thats like how do you determin the conc of [creatine] in urine sample using your calibraion curve?

1. Use same volumes of solutions as used in producing (calibration curve)

2. Read off (creatinine) concentration against absorbance/transmission (value) obtained;

Ignore 'line of best fit'.

Accept 'compare' for 'read off

what bit acc is the nephron?

the whole vagina penis looking thing - like with all the bits - and wehere ultrafiltration sleective reabsortion bla occurs...

the DCT and PCT are which bits if were going to describe them?

PCT = the first little loop bit of the long lighter grey string - tighly looped

DCT = less tighlty looped second bit - and op right of vag shape

where does diagra of structure of nephron split between cortex and medulla - cortex is upper layer

just under PCT

whats the PCT?

proximal convoluted tubule

- a series of loops surrounded by capillaries

- reabsorbtion of glucose and AA's b

bowmans capsule?

at start of nephron

- surrounds a bundle of glomerular capillaries called the glomerulus

[ is like the golf ball shaped thing]

Afferent arteriole

carries blood to the glomerulus

blood going IN to bow mans capule

supplies nephron with blood from renal artery

whats the loop of henle? has to what?

the long, hairpin loop

- extends from cortex into medulla

- surrounded by capillaries

HAS ASCENDING [ impermeable to water} AND DESCENDING LIMB {highly permeable to water}

efferent arterioel

e = exit - carries blood away from bowmans caplsule

DCT?

similar to PCT

- role to reabsorb ions and some water

collecting duct?

DCT empties filtrate here

ADH effects the permeability of collecting duct and so is vital to osoregualtion

- is the tree trunk looking bit on right hand side

- and turns the filtarte into urine - and urine taken to bladder via the ureter

glomerular capillary

fulid [filtrate] is forced out of capilaries though pores - due to high hiydrostatic pressur e

names the things in the strcure of nephron

- afferent arteiole

-efferent arteriole

-Gloerular capillary

- bowmans capsule

-PCT

-DCT

- loop of Henle

- blood capilaries

-collecting duct

after entering the renal artery, blood enters the what? in which arteriole? where it divides to form what? these capilaries then rejoin to form what?

bowmans capsule

Afferent arteriole

cappilaries that make up the glomerulus

the Efferent arteriole

[so baso afferent art to glom capillaries to efferent art - the aff/eff are just the fat single ones - and when all the glom caps are bundled up together in bows cap this = the glomerulus ]

what are glomerular cappilary walls made up of?

endothelial cell walls with pores/fenestrations [so small molecules can move out]

what are the 4 steps in production of urine?

1. formation of glomerular filtrate by ultrafiltration

2. selective reabsorbtion of gluose and AAs and water by proximal convoluted tubule

3. maintaining a gradient of sodium ions in the medulla by the loop of Henle

4. reabsorption of water by the distal convoluted tubule and collecting ducts

STEP 1 - in formtion of urine - how does ultrafiltration produce glomerular filtrate?

1. diameter of afferent arteriole wider than efferent causing HIGH HYDROSTATIC PRESSURE

2. so small molecules are forced from the capilary through gaps/fenestrations to form the gloerular filtrate

3. blood cells and larger proteins cnnot pass through as they are too large

ultrafilytration v scheve exav q

1. High blood/hydrostatic pressure;

2. Two named small substances pass out eg water, glucose, ions, urea; Accept correct named ions Accept mineral ions/minerals Accept amino acids/small proteins Ignore references to molecules not filtered

3. (Through small) gaps/pores/fenestrations in (capillary) endothelium; Accept epithelium for endothelium

4. (And) through (capillary) basement membrane;

name 5 of the small molecules that can pass through?

urea, water, AA's, glucose, ions

describe how ultrafiltration occurs in a glomerulus? exam q

1. high blood/ hydrostatic pressure

2. so water/glucose/ions/urea/ AAs pass out

3. through small gaps/pores/fenestartions in capillary endothelium

4. and through capillary basement membrane

descrie how ultrafitartion produces glomerular filtrate exam q - exact mark scheme

1. blood/hydrostatic pressure

2. small molecules/named example

3. pass through basement membrane/ basement membrane acts as a filtarte

4. proteins too large to go through/so stay behind

5. presence of pores in capillaries/ presence of podocytes

what are the 3 diff layers that filtarte has to pass through?

1. small molecules pass through pores in capillaries endothelial cells

2. basement membrane

3. spaces between podocytes

describe a bit more the basmment ebane and podocytes

- the basemenet membrane is made of like collagen and other proteins - dont nneed to know - and acts like a sieve

- with the clawclip analogy - the beaseent mmemmbrane is the tissue paper around the capilarly tube

and the podoctyes - the flitrate passes BETWEEN podoctyes not through themm

- and so podoctyes are like the claw clip claws - - they actually are just like little blobs with gaps between the blobs

what are 4 adaptation of the PCT?

1. epithelial cells have microvilli = large SA for reabsorption = because increased SA = 1. more channel/carrier proetin channels for fac dif +co transpport and 2. more carrier proetisn for active transport

2. infoldings at their base = increase SA for reabsorption into blood [ like the microvilli the cheese string head and infolding re just bigger loops]

3. high density of mitochondria (to produce ATP for active transport - sodpotaspummp)

4. also many ribosoes/RER = to produced carrier/channel proteisn

so in the step 2. procees of selective reabsorption of glucose and AAs and water by porximal convoluted tubule - what is and isnt reabsorbed?

useful sustances required by body are - but waste products such as urea arent

what are the 4 steps please in the process of selective reabsorption of glucose and AAs and water by the proximal convoluted tubule? [btw its the same idea s cotransport of glucose from the ileum}

1. sodium ions are actively rranpsorted/pumped out , reducing their conc [in epithelial cells] [ 3na out - 2 k in - and this maintains a conc gradient for na into the epithel cell of the PCR ]

2. sodium ions diffuse down conc gradient [fac dif] from the lumen of the proxial convoluted tubule through co-trnsport proetins which carries other molecules with it [eg glucose and AAs]

3. glucose/AAs move by fac dif into the blood through a channel proetin [basal membrane of PCT epithelial cells}

4. water enters blood via osmosis - down a water potential gradient

how would you describe the shape of the loop of henle?

hair-pin shaped tubule - that extends into the medulla of tyhe kidney

what is the loop of henle responcible for ? / aim

for water being reabsored from the collecting duct[back into surrounding blood capilaries] , which concentrates the urine so it has a lower water potential than the blood

so baso aim is to reabsorb water from the collecting duct - making the urine more concentrated

WHAT Is directly related to the loop of Henle ?

the concentration of urine produced - so the longer the loop of henle, the more water can be reabsorbed back by osmosis = a small volue of very concentrated urine - e,g cammels/desert animmals

what are the 2 regions of the loop of henle? and describe

1. descending limb: narrow, thin walls, highly permeable to water [therefore water leaves the filtrate and goes into the blood]

- ascending limb: wider, thick walls, impermeable to water [ na is pumped out from filtarte]

whats the most iportant thing to say about the loop of henle? think of like fish adaptation

tje loop of Henle acts as a !!!counter-current multiplier!!! and hence maintains a water potential gradient for the whole length og the collecting duct

why would graph of concertration of filtrate peak [goes up and down] in the loop of henle compared to PCT, DCT, COLLETCING DUCT ETC - exav q

1. conc rises in descending becauses water out anf sodium in

2. conc lost in ascendng limb because sodium and chloride ions are actievly removed

3. but water remains as ascending limb walls are impermeable

exam q - why thicker kidney medulla = steeper conc of urine

1. thicker medulla = longer loop of henle

2. the longer the loop of henle - means increase in na+ ion conc in medulla/na+ ion gradient maintained for longer/ more na+ ions are moved out int the medulla

3. therefore water potential gradient vaintained for longer, so more water reabsobed fom loop and collecting duct by osmosis

talk about conc of sodiuv ions or solute? - vark scheve exav q

1. Concentration rises in descending limb because sodium ions enter and water lost;

2. Concentration falls in ascending limb because sodium ions (and chloride) ions actively removed;

3. But water remains (in ascending limb) because its walls are impermeable (to water).

why does habiing longer loop of henle and more ADH secreted make better adated to living in desert conditions?

general:

- more water reabsorbed [to blood]/less lost in urine

- by osmoisi

- from collecting duct

loop of henle:

- sodium/chlrlodie ions absored from filtrate in ascending limb

- gradient established in medulla/ conc of ions increases down medulla

adh:

- acts on collecting duct/DCT

- makes cells more permeable/inserts aquaporins in plasm membranes

osmolarity =

conc of solute/solution

please describe process 3 - mainaining a gradient of sodium ions in the medulla [interstitual tissue] by the loop of henle - this IS THE BIG PAGE OF WRITING - with like 8 steps and waht we watched that complicated video of - FIFURE OUT ARK SCHEME AND REDUCED WHAT ACCUAL NEEC TO KNOW VERSION OF THIS BECAUSE THIS IS TOO MUCH ISTG

1. sodium ions are actively transported out of the ascending limb, using ATP [somme na diffuses straight back into descending limb]

2. this generates a lower water potential [more negative] in the region of the medulla between the 2 limbs - interstitial region. Thick walls so impermeble to water so very little escapes

3. however the descending limb are very permeable to water so water moves out of the filtrate by osmosis. this water then enters the capilaries by osmosis(back to heart via renal vein)

4. the filtrate progressivly loses water, lowering the water potential inside the tubulr. it reaches the lowest water potential [ most neg/ highest osmmolarity] at the hairpin

5. at the base of the ascending limb, na+ diffuses out and are also actively pumped out further up the limb, making the water progresively less negative (more hypotonic/lower osmolarity/less solute)

6. there is a gradient of water potential between the ascedning limb and colletcing duct with the highest water pot [lowest osmolarity] in the cortex and increasingly lower water pot [higher osolarity] as you go further into the medulla

7. the collecting duct is permeable to water so as the filtrate moves down it, water passes out by osmosis. this water moves into surrounding blood cappialrie and is carried away [t renal vein].

8. as water passes out of the filtrate = lowers water pot. however, water pot of interstitial fluid is also lowered and so water continues to move out by osmosis down whole length of collecting duct = counter current multiplier effect

please describe proccess 4 - reabsorption of water by the distal convoluted tubule and collecting ducts

- first part of DCT = same function as ascending loop of Henle = reabsorption to blood of ions [final adjustment to ion conc of blood]

- second part of DCT = same function as collecting duct = water reabsorption into the blood, and DCT contains ADH receptors on the CSM[like collecting duct]

- cells that make up the walls of the DCT have many microvilli and many mitochrondira that allow them to reabsorb material rapidly from the filtrate by active transport [low to high conc against conc gradient ]

- overall role of DCT is final adjustments to water and salts that are reabsorbed [to the blood]and control ph of blood by selecting which ions are reabsorbed

what is osmoregulation?

the control of blood water potential

what 2 things is the water potential of blood consequences of?

the solutes [eg AAs, glucose, ions, urea, ] plus the volume of water

so for that page on the effects of osmoregulation - with the tables - one half orange the other blue - whats the order of steps [basic names]

1. stimulus, 2. causes, 3. receptor, 4. coordinator, 5. effector, 6. response, 7. consequences on target cells

so for that page on the effects of osmoregulation - with the tables - one half orange the other blue - whats the order of steps for FALL IN WATER POTENTIAL OF THE BLOOD [ie more concentrated/negative water potential]

1. stimulus,= fall in wp of blood

2. causes, = too many ions/too little water being consumed and or overheating so a lot of sweating

3. receptor, = cells called osmoreceptors in the hypothalamus of the brain detect the decrease of wp of blood and so ater is lost from osmoreceptors into the blood by osmosis

4. coordinator,= the hypothalumus sends more impulses to the posterior pituitry gland

5. effector, = posterior pituitary gland

6. response, = more ADH released into the blood

7. consequences on target cells = more ADH travels in the blood to the kidney where it increases the permeability[more aquaporins] of the distal convoluted tubule and collecting duc to water - and so more water is reabsorbed into blood by osmosis from the collecting duct = smaller volume of urine = more concentrated urine = conserves water

so for that page on the effects of osmoregulation - with the tables - one half orange the other blue - whats the order of steps for RISE IN WATER POTENTIAL OF THE BLOOD [ie more dilute/ less negative water potential] OPPOSITE to fall

1. stimulus,= rise in wp of blood

2. causes, = large volume of water being consumed and salts used in metabolism and excreted but not replaced from diet

3. receptor, = cells called osmoreceptors in the hypothalamus of the brain detect the increase of wp of blood and so water enters osmoreceptors from the blood by osmosis

4. coordinator,= the hypothalumus sends fewer impulses to the posterior pituitry gland

5. effector, = posterior pituitary gland

6. response, = less ADH released into the blood

7. consequences on target cells = less ADH travels in the blood to the kidney where it decreases the permeability[less aquaporins] of the distal convoluted tubule and collecting duct to water and urea - and so more water is reabsorbed into blood by osmosis from the collecting duct = larger volume of urine = more dilute urine = removes excess water

so if your dehydrated would you have more or less ADH?

MORE!

Please can you describe what the impact of ADH is on the collecting duct - remember this is what i learnt on seneca....

1. protein receptors on CSM of DCT and colletcing duct bind to ADH, leading to phosphorylase enzyme activation

2. phosphorylase causes vesicles containing aquaporins [ specific channel proteins for water] to fuse with the cell membrane of the DCT and collecting duct

3. more aquaporin channels = increases the permeability of DCT and collecting ducts to water and therefore more water leaves the collecting duct via osmosis [ more water is reaborbed into the blood]

EXTRA = ADH also increases urea permeability so more urea also leaves, lwering the wp of interstitial region

- both recombine to mean more is reabsorbed from the filtrate into the blood via osmosis resulting in more concentrated urine and a smaller volume

describe fall in wp shortly - from that cute diagram of osmoregulation summary

1. too little water - reduced water intake increase sweting, slat intake

2. decreased water potential of blood ie a high solute conc

3. fall in wp detected by osmoreceptors in hypothalamus

4. the DIFFERENT PATHWAY IS THAT - STIUMULATION OF THRIST CENTRE IN BRAIN = MORE WATER CONSUMED

4. but otherwise pituitary gland release more ADH

5. walls of DCT and collecting duct become more permeable to water

6. less water leaves the body and urine is therefore more concentrated - and normal wp of blood now

AND TOO MUCH WATER IS JUST OPPOSITE X - but without the thirst centre

so please describe the curve on the graph - where it increases and the water pot is too high and there is too much water

1. WP increases due to over hydration

2. detected by osmmmoreceptors

3. fewer impulses [hypothalaumus to pituitray gland]

4. less ADH

5. DCT and collecting duct less permmeable to water

6. less water reabsorbed

7. large volume of dilute urine