Renal Handling Of Na K And H20

Front 1

what are the two pathways by which materials can leave the urine compartment
which is active and passive?

Back 1

paracellular pathway (passive transport driven by gradients)
transcellular pathway movement through the cell - 2 steps - Na enters the apical membrane and then has to leave the cell across basolateral membrane (active) entry is usually passive and exit is usually active

Front 2

what are the two sides in reabsorption

Back 2

a urine side and a interstitial side

Front 3

describe sodium gradient inside/out of cell

Back 3

intracellular content of Na is low
Na in urine is very high (15 vs 145)
strong gradient for Na to enter cell
there is an electrical and chemical gradient drwaing Na inside,- negative resting potential of the cell (-70 mv)

Front 4

is the entry step of Na passive or active

Back 4

passive - chemical and electrical gradient

Front 5

is the exit step of Na p or A

Back 5

active- N/K ATPase pump- have to overcome chemical and electrical gradients

Front 6

where does the bulk of Na reabsorption occur

Back 6

proximal tubule- 2/3
another major site - loop of henle -25%
both account for about 90%
remainder in distal tubule and collecting duct

Front 7

how much of the Na is reabsorbed

Back 7

about 99%

Front 8

what are the two parts of the proximal tubule

Back 8

early and late
pertains to how Na is reabsorbed

Front 9

whatare the major transporter for Na reabsorption in early proximal tubule

Back 9

Na/H+ exchanger (linked to bicarb reabsorption)
also have Na/solute cotranspoter (glucose aa, phosphate, lactate)
realize Na reabsorption is linked to other reabsorption

Front 10

what solutes are reabsorbed to the greatest degree in Proximal tubule

Back 10

glucose, aa, HCO3- most reabsorbed by halfway mark of PT
Na reabsorption in latter half is linked to CL

Front 11

how is Na transported in the late proximal tubule

Back 11

parallel exchanger Na/H and Cl/base
this allows continuation of Na reabsortion despite disappearance of organic molecules

Front 12

by the time the tubular fluid reaches the end of the proximal tubule how would you describe it

Back 12

it is an elctrolyte solution
initially identical to plasma, but by the time you reach end of PT- have Na, K, Cl, Mg

Front 13

where does Na reabsorption occur in the loop of henle

Back 13

ascending limb -
some reabsorption in thin limb
the majority of the 25% occurs in the thick ascending limb

Front 14

what is the transporter responsible for Na reabsortion in asceding loop of henle

Back 14

cotransporter Na/K/2Cl
only one now b/c PT has cleared filtrate of all other solutes

Front 15

distal tubule early segment transporter Na

Back 15

Na/Cl co transporter - 5%

Front 16

whats the difference between PT, LH and early distal tubule vs late distal tubule and collecting duct

Back 16

they all have cells with transporters to reabsorb na as you enter latter distal tubule and collecting duct, na reabsorption is limited to a specific cell type,

Front 17

what is the specific cell type that is responsible for Na reabsorption in late distal tubule and collecting duct
what is the other cell type

Back 17

principle cell- 70% of LDT and CD
intercalated cell - not involved in Na reabsorption

Front 18

what is different about the sodium transport of principle cell

Back 18

not a cotransporter or exchanger, it is a conductive pathway
ENAC- Epithelial Na channel
moves out of the cell via Na/K/ATPase

Front 19

2 categories- those that stimulate Na reabsorption- decrease Na excretion

Back 19

antinatriuretic agents

Front 20

what are antinatriuretic agents and what is their mechanism of action

Back 20

NE- NT released from sympathetic nerves - also targets Na/K/ATPase (so affects Na movement on both sides)
angII
target specifically PT
they act on Na H exchanger (b/c major site of reabsorption)

Aldosterone - targets principle cell - late distal tubule ancd collecting duct

Front 21

how is aldosterone different from NE and ang Ii

Back 21

aldosterone doesnt have a membrane receptor, it can cross cell membrane (it is a steroid) it binds to a intracellular minerallocorticoid receptor. This complex migrates to the nucles and promotes tc of aldosterone induced proteins- stimulate more Na channels that is inserted into apical membrane, and also Na/K/ATPase in bsasolateral membrane. also targets mitochondria and boost enzymes to help ensure that there is enough energy for Na/K/ATPase

Front 22

what hormone decreases Na reabsorption
and where does it work

Back 22

ANP- atrial natriuretic peptide. targets later part of nephron- principle cell.
activity due to changes in conduction of Na chanel

Front 23

describe change s in Na by ANP

Back 23

there are ANP channels on basolateral membrane of principle cells, it triggers production of CGMP:
cGMP inactivates ENAC by binding to allosteric modifier site on channel or
by phosphorylating the channel cGMP dep PK



GMP can bind to chanel to reduce activity or it can activate a phosphorylation process that will also reduce Na chanel. net affect is a decrease in Na handling by P cell through ANP. Causes more Na excretion

Front 24

what are natriuretic agents

Back 24

increases Na excretion

Front 25

pharmacological agents that are designed to block Na reabsorption

Back 25

diuretics - b/c Na reabsorption is linked to water- increasing urine - diuresis
no affect on water

Front 26

loop of henle Diuretics and MOA

Back 26

loop diuretics- interefere with Na/K/2Cl- triporter
bind to specific binding site. the diuretic bind to the Cl binding site. Now transporter is inactive and no longer transports Na. b/c Na reabsorption is 25% in LOH, loop D is powerful. b/c of diuresis, consequence is drop in BP or hypotension

Front 27

early distal tubule diuretics

Back 27

thiazide diuretics- targets Na CL transporter, binds to Cl site. transporter becomes inactive.
consequence - increase in Na and H20 excretion - drop in BP
also fairly effective

Front 28

late distal tubule and collecting duct

Back 28

K sparing duretics
binds to Na channel of P cell- less Na being reabsorbed

Front 29

whats the link between Na reabsorption/excretion and water

Back 29

increase Na reabsorption - secrete out less water
decrease Na reabsorption- secrete out more water
water reabsorption is guided by the gradient produced by Na reabsorption

Front 30

what 2 segments of nephron are permeable to water and why

Back 30

proximal tubule
thin descedning limb of LOH
both apical, basolateral membrane and tight junctions are permeable to water

Front 31

what parts are impermeable to water

Back 31

ascending loop of henle, distal tubule and collecting duct
it will not transport water on its own

Front 32

how does Na reabosrption aid water reabsorption

Back 32

osmolality of tubular fluid will decrease as Na is reabsorbed but increases it on the other side into the interstitiatl compartment sets up osmotic membrane

Front 33

how much water is reabsorbed in each segment

Back 33

67 in PT
15% in LOH confined to descending limb
the osmotic gradient is set up by Na being reabsorbed by ascending limb- increases osmolality in the interstitium

Front 34

can the water permeability of lDT and CD be changed
and how

Back 34

yes, through the action of ADH (vasopressin) inserts water channels into apical membrane of LDT and CD, water entering here will now be reabsorbed. in max ADH- urine output will be 500- 700 ml
can regulate amount of urnine by ADH

Front 35

principle cells and ADH

Back 35

they interact with ADH and water permeability of P cells is altered by ADH
they normally have water channels but only on basolateral sides. tehy are contained in vesicles just below the membrane.
ADH forces isertion of water channels into apical membrane.
the higher the concentration of ADH- more water channels are inserted.
as soon as ADH levels drop- the channels are interanalized- and those cells become water impermeable and water reaabsorption ceases

Front 36

in what situation can you rpoduce 15-20 L of urine a day

Back 36

where the distal portions are impermeable to water-
dont produce ADH or dont produce any water channels
they suffer from DI
central- no ADH production - water impermeable distal portions
nephrogenic- dont have receptors in P cells or no manufacturing of these channels

Front 37

K is filtered and reabsorbed but can also be excreted by changes in transport by a certain segment. where is K reabsorbed

Back 37

PT and Lof H- 80% and 10%
if you are on a low K diet- then the DT and CD will continue to reabsorb K and be putting out very little K
normal diet is high in K, the PT and loop of Henle still reabsorbs - 90% but the DT and CD can excrete large amounts of K

Front 38

how does DT and CD excrete K

Back 38

kidney switches from K reabsorption to secretion
have 2 population of cells
principle and intercalated cells
PC- are involved in K excretion
if there is low K diet
intercalated cells - reabsorbs and conserves remaining K