3.6.4.3 - control of blood water potential

function of the kidney

excrete waste via filtration of blood, maintain water, hormones

ultrafiltration

blood in glomerulus separated from bowman’s capsule by capillary endothelium, basement membrane and podocytes (bowman’s capsule endothelium cells), efferent arteriole narrower than afferent arteriole, hydrostatic pressure forces fluid out of blood, all blood cells and large plasma proteins maintained, proteins left in blood give blood very low water potential, ensures small amount of water left in capillaries, fluid entering PCT contains nearly all glucose/ions/urea/water that entered glomerulus

basement membrane

mesh of collagen and glycoprotein, ensures that only molecules with mr less than 69000 can pass through

podocytes

specialised structure with finger like projections (processes) which wrap around the capillaries, ensuring there are ‘gaps’ for fluid to flow (do not affect fluid filtering)

what happens when larger molecules pass through basement membrane

they are reabsorbed into blood via endocytosis, requiring energy from atp

where does selective reabsorption occur

proximal convoluted tubule

how is the pct adapted for its function

tightly wound to increase sa, lined with specialised epithelial cells containing microvilli and basal interdigitations, lots of mitochondria for atp for at, surrounded by capillaries to maintain conc gradient - all increase rate of diffusion

process of selective reabsorption

na+k+ pump removes na from pct lining cells which changes conc of na in cytoplasm, na+ drawn into lining cells from pct due to conc gradient, only way for na to enter cell is with glucose or amino acid (co-transport), conc of amino acids and glucose in lining cells increases, glucose and aas diffuse out opposite end of lining cell into capillary, removal of glucose, salts and amino acids increases pct water potential, so water leaves by osmosis, 100% glucose reabsorbed via symport + at and 70% of water and ions via at

why does the concentration of the filtrate not change in selective reabsorption

only volume changes, we lose solute and solvent at the same rate as water chases solutes out into the capillary

urea formation

excess aas from diet go to liver for deamination (removal of n), this is converted to ammonia then to urea, rest of aas stored as fat

loop of henle

extends into medulla of kidney, responsible for water being reabsorbed from collecting duct, thereby concentrating the urine, conc of urine produced related to length of loop of henle

ascending limb of loop of henle

na+ ions diffuse out at base and as it moves up, na+ ions actively transported out using atp from many mitochondria in lining of its wall, filtrate water potential increases, low water potential in interstitial region, water cannot follow after because walls impermeable to water

descending limb of loop of henle

walls permeable to water so passes out of filtrate down water potential gradient by osmosis into interstitial space then into blood capillaries to be carried away

interstitial space

region of medulla between 2 limbs, gradient of water potential with highest water potential in cortex and increasingly lower water potential the further into the medulla it goes

collecting duct

permeable to water, as filtrate moves down water leaves via osmosis into tissue fluid then into blood vessels and is carried away

how does the loop of henle act as a counter current multiplier

ensures there is always a water potential gradient drawing water out of the tubule, so as water leaves filtrate water potential is lowered but water potential in interstitial region also lowered so water continues to move out via osmosis down whole collecting duct

distal convoluted tubule and collecting duct

responsible for reabsorption of ions such as na+

osmoregulation when water content of blood too low due to too much salt or sweating

osmoreceptors detect low water potential in osmoreg centre in hypothalamus, posterior pituitary gland releases more adh, adh travels via blood to pct and cd, more adh increases no of aquaporins in dct and cd cell membrane so more permeable to water, increased volume of water reabsorbed into the blood, low urine output (small vol of conc urine), water content of blood returned to normal

osmoregulation when water content of blood too high due to too much water drunk

osmoreceptors detect high water potential in osmoreg centre in hypothalamus, posterior pituitary gland releases less adh, adh travels via blood to pct and cd, less adh decreases no of aquaporins in dct and cd cell membrane so less permeable to water, decreased volume of water reabsorbed into the blood, high urine output (large vol of dilute urine), water content of blood returned to normal

where are osmoreceptors found

right atrium and carotid sinuses, detect pressure/volume drops

second messenger model for adh

adh binds to trans-membrane receptors on basal/capillary side and changes protein shape and activates adenyl cyclase, causes atp to be converted to cyclic amp which activates protein kinase, this phosphorylates intracellular enzyme phosphorylase, activated phosphorylase triggers vesicles containing aquaporin to move to lumen side and fuse with cell membrane, more pores opened up so water moves into cell down water potential gradient out of cell into interstitial fluid then the blood