can either be passive (down electrochemical or osmotic gradient) and active (against electrochemical gradient with glucose adn Na+)

basolateral membrane has basolateral pump and 80% of kidney energy spent

pump transports Na+ out of tubular cell into lateral space, and the high concentration in lateral space means Na+ diffuses into interstitial fluid and into peritubular capillary

the K+ moves back out of tubular epithelial cell through leaky channel; and Cl- moves down electrochemical gradient, created by active reabsorption of Na+, and passes between tubular cells not epithelial cells

67% proximal tubule is linked to reabsorption of glucose, amino acids, water, Cl- and urea

8% under normal hormonal control is linked to long term control of blood pressure an dis linked, in part, with K+ secretion

It promotes Na+ reabsorption in response to circulating ANGII acting on adrenal cortex

it inserts Na+ leak channels into luminal membranes in principal cells, so increase Na+ reabsorption by kidney tubules

Renin-angiotensin-aldosteron esystem controls aldosterone secretion

liver secretes angiotension and kidneys secrete renin to angiotensin 1 (inactive) which is then converted to angiotensin 2 (catalysed by enzyme from lungs) (active)

it also increase Cl- and more water is conserved (since Na+ osmotically holds more water) so impacts blood pressure and ECF volume

they inhibit renin secretion by kidney adn aldosterone from aldosterone secretion

if sodium is retained then blood pressure increases so the heart stretches more, this degree of stretch control their release- atria release ANP and ventricle release BNP (ANP more effective than BNP)

overall effect is reduced blood pressure since reduced Na+ load and thus reduced fluid load, it also reduce peripheral vascular resistnace by inhibiting sympathetic NS to heart and blood vessels

symport carries Na and glucose cotransporter allows passive Na+ across luminal membrane and basolateral pump moves Na+ into lateral space

this pulls glucose through SGLT against concentration gradient

passive diffusion down concentration gradient across basolateral membrane into plasma through faculative carrier glucose transporter

water passively moves through tubule becasue of movement of Na+

absorbed in proximal tubule (65%) and descending limb of LoH (15%)

water can either move between cells or through water channels

urea concentration in filtrate=plasma urea concentration so no net movement of urea

extensive reabsorption of water reduces volume so increase concentration by end of proximal tubule, which creates concentration gradient between filtrate

tubule walls are not fully permeable so 50% reabsorbed but usually adequate removal

they have microvilli on apical surface to increase surface area for reabsorption and have many mitochondria since metabolcially active

more 75% of fluid that intiially enters the nephron is reabsorbed but the overall osmolarity does not change so it is isomotic reabsorption

there is active absorption of K+ without regulation and then goes straight into blood stream since ECF has relatively small K+ concentration as 98% of K+ is in intracellular fluid

filtered K+ is almost completely reabsorbed in prosimal tubule meaning any K+ in urine comes from secretion

a Na-K pump establishes a gradient so that potassium diffuses out of the blood into the interstitial fluid

The ATP channel then pumps K into the principal cell and the presence of leaky channels means K moves into the lumen

when K+ levels are low the secretion is low since electrochemical gradient needs to be maintained

when K+ levels are high the secretion in distal nephron is increased so just enough is added to filtrated to reduce plasma K+ to normal

Mechanism Na+ is transported to lateral space from principal cell and K+ moves into principal cell from lateral space (Na-K pump)

the high intracellular concentration of K+ favours net movement into the tubule lumen with passive diffusion through K+ leaky channels

the interstitial fluid concentrations of K+ is low so passive movement out of peritubular capilalry plasma nad basolateral pump actively induecs net secretion of K+ from peritubular capillary into tubular lumen

Aldosterone increases K+ secretion since it promotes insertion of Na channels in distal and collecting tubule

aldosterone is stimualted by rise in plasma K+ level which promotes tubular secretion so more K+ in urine

Low Na+ triggers renin angiotensin system to produce aldosterone (drinking lots of water can lower Na+ concentration so more K+ is excreted)

the fluid that enters the LoH has the same osmolarity as teh blood plasma (isotonic with surrounding fluid)

water flows osmotically out of the descending limb into more concentrated fluid until equilibrium

water moves through AQ1 on luminal surface then AQ2 on basolateral

NaCl is actively transported out to establish 200mOsm/L gradient

this creates a vertical gradient osmolarity that is larger at the bottom of medulla than cortex

it makes tubular lumen walls more permeable to water by the insertion of aquaporins

V2 receptor (in blood vessel) and V1 (on basolateral surface) to exert vasoconstrictor effect

aquaporins are stored in vesicles ready for release and type 2 are inserted in luminal side

osmoreceptors are stretch sensitive neurones that increase fire rate as osmolaroty increase, so high salt concentration increase vasopressin release

need a 4% change in plasma osmolarity to stimulate a need to drink

cells shrink and nonspecific cartionic channles linked to actin filaments open which depolarises the cell but are only activated above 280mOsm

lots of vasopressin is released to produce concentrated urine in mourning

nocturnal enuresis is reduced vasopressin secretion and results in bed wetting

water moves by osmosis into interstial fluid

fluid entering distal tubule is less osmolarity than its surroundings (hypotonic), and there is still 20% filtered water in lumen for variable reabsorption

filtrate osmolarity decreases from 1200mOsm to 100 mOsm from medulla to cortex

the luminal side contains ion symporters which pulls in Na+, then K+ and Cl- follow. The Basolateral side has a Na-K ATPase to pump Na out and K+ and Cl- leaky channels

The NKCC symporter uses energy stored in Na+ concentration gradient to transport Na+ K+ 2Cl- from lumen to epithelial cell

NKCC mediated transport can be inhibited by loop diuretics Furosemide

transport of solute out of ascending limb dilutes filtrate and increase interstitial fluid concentration

Water leaves the tubule to enter the vasa recta if an osmotic gradient exists between the medullary interstitum and vasa recta

At the bottom of the loop of Henle osmolarity is 1200mOsm which is equal to interstitial fluid

blood flows back to the cortex with high plasma osmolarity which attracts water lost from the descending limb

deep in the medulla it loses water and picks up solutes from the ascending limb

this means that plasma osmolarity decreases while preventing water dilute interstitial fluid

cannot generate enough bicarbonate so kidneys massively reabsorb bicarbonate (in Type A I cells)

hypoventilation means CO2 is retained adn H+ and bicarbonate levels are elevated

diets increase H+ input or lactic acid builds up or ketoacidosis (excessice breakdown of fats or certain amino acids)

excessive vomiting of stomach acid or excessiveingestion of bicarbonate antacids reduces H+ and CO2 and increases bicarbonate

the body tries to compensate with hypoventilation and by excreting bicarbonate and reabsorbing H+