How does water get made to move?
What are the 2 different types of pressure?
Hydrostatic pressure and osmotic pressure
Why do vasa recta get a lower hydrostatic pressure?
Because a lot of hydrostatic pressure is lost at the glomerulus
What drives GFR?
Hydrostatic pressure which is controlled by afferent and efferent arteriole diameter.
Osmotic pressure controlled by transport of solutes to set up an osmotic gradient and selective water-proofing (aquaporins and ADH)
What does glomerular filtration result in?
blood that does not contain any cells, protein complexes, and >50 kDa proteins
What does GFR depend on?
Permeability of membrane
Surface area of membrane
What determines filtration pressure?
Glomerular blood hydrostatic pressure drives filtration out of the glomerulus and osmotic pressure back into the glomerulus
How is glucose transport done into the cells from the lumen during reabsorption?
Glucose concentration within cell is kept high by co-transporting glucose with sodium into the cell and then opening glucose transporters on the other side to go down the concentration gradient that was created. Most of this happens in the PCT
How do we sense BP?
Stretch receptors (barorececeptors that sense stretch decrease and stimulate noradrenaline release) Atrial mechanoreceptors which sense increase in stretch and release ANP Afferent arteriole stretch (sense myogenic autoregulation)
(Osmoreceptors sense increase in osmolarity of blood and release ADH)
Kidney function (tubuloglomerular feedback)
What do mesangial (macula densa) cells produce?
How is GFR maintained?
Myogenic autoregulation (works well both ways)
AtII (complex; it constricts both arterioles to maintain GFR)
What does ANP do?
Dilates Aff and constricts Eff to produce more GFR
Tubuloglomerular feedback (movement through kidney is too slow means low BP which interpreted as low salt at DCT and so Afferent arteriole is dilated increasing GFR.
How does the sympathetic NS affect GFR?
It constricts AA and decreases GFR dramatically
How does reabsorption get increased?
RAAS (AtII and aldosterone increase Na reabsorption and water follows increasing BP)
ADH opens up CD/CT aquaporins causing water to be reabsorbed
How does reabsorption get decreased?
ANP Blocks Na+ reabsorption and water follows
What happens when there is high amounts of aldosterone?
Potassium is leached
Where is most AtII activity taking place?
At the afferent arteriole and the Proximal Convoluted Tubule.
AtII does affect DCT but not as much as PCT. Aldosterone does most of the work.
What is NorAdrenaline’s effect on the Afferent arteriole?
Why can AtII act as a dipsogen?
It can pass the blood brain barrier through leaky tight junctions and interact with the receptors
Why does AtII constrict afferent arteriole?
MAP is increased all around the body so it is a compensatory mechanism