Lecture 9 - ATP Pumps and Ion Exchange Flashcards
what are the functions of the sodium pump ?
forms the key Na+ and K+ gradients
needed for flow of K+ and Na+ in setting up resting potential
secondary active transport
use of Na+ as a H+/glucose co transporter
this allows maintenance of PH
control of intracellular calcium conc - 10000 fold difference across the plasma membrane - cells singal by very small changes in the intracellular Ca2+
- this allows for a rapid response
outline the receptors involved in controlling the intracellular calcium rate
ca2+ at 2mM outside cell and 10-7M inside cell
on the PLASMA MEMBRANE
PMCA - Ca2+ ATPase - uses ATP to push 1 Ca2+ out and 1 H+ in
high affinty , low capacity - cant move too much ca2+
NXC - Na+ - Ca2+ exchanager - 3Na+ in for 1 Ca2+ out
low affinty - high capcity - can move lots of Calcium when at high concs
Flows down Na+ gradient
sodium pump provides the extracellular Na+ conc for the NCX channel to function
If needing to raise cellular Ca2+ conc the NCX exchanger can work in reverse to pump calcium into the cell - if the cell has become depolarised
ROC - receptor operated Ca2+ channel, lets Ca2+ FACIL DIFF when a signal opens gated channel
VOCC - Voltage sensitive Ca2+ channel will open to let Ca2+ in when conditions are met
ON THE SARCOPLASMIC RECTICULUM
conc of Ca2+ higher in the SER than the inner cell
SERCA channel - Ca2+ - ATPASE - 1 Ca2+ in to SER for 1 H+ out of the SER - uses ATP
CICR - Calcium induced calcium release channel - when ca2+ is high in the cell it can bind to CICR to open this gated channel , allowing Facil Diff of calcium from SER into cell - raises cellular ca2+ conc
IP3 receptor - Signal binds ie from a g protein - opens channel allowing ca2+ to enter cell from SER, raising Cellular calcium levels
Store operated calcium channel - SOC - between cell exterior and inside of SER allows the SER to draw in Ca2+ from outside the cell !
MITOCHONDRIA -
Ca2+ uniporters bring Ca2+ from cell into the Mitochondril membrane
when needing to raise cellular Ca2+ - Ca2+ uniports push calcuim out of mitchondria into the cell
how do we raise the Ca2+ cellular concentration ?
Facilitated diffusion ROC from outside to inside cell VOCC - voltage operated Ca2+ Channels IP3R receptors from SER CICR from SER - ryanodine receptors SOC pulls Ca2+ from outside cell into SER to replenish Ca2+ levels Mitochondrial Ca2+ uniporters
Secondary active transport
NCX - can be reversed to bring in Ca2+
How do we maintain resting Ca2+ conc ?
Ca2+ 2mM OUT - 10^-7 IN
Sodium pump maintian external Na+ conc to allow secondary active transport
Secondary Active transport
NCX removes CA2+ for 3NA+ in - low affinty, high capacity - removes most the ca2+
Primary active transport
PMCA uses ATP to drive Ca2+ out - high affinty low capacity - removes residual Ca2+
SERCA on SER use ATP to Push Ca2+ into SER and one H+ out of SER into the cell -high affinty low capacity - removes residual Ca2+
Facilitated diffusion
Mitochnodrial uniporters remove Ca2+ from inside cell
operate at high Ca2+ to buffer damaging levels of Ca2+
How is NCX affected in ischameia
Ischamea - patient has depleted ATP and low O2
sodium pump no longer works - cannot set up Na+ gradient
Na+ builds up in the cell
the NXC reverses to drive Na+ out Ca2+ in
high levels of Ca2+ are toxic
how do we control our cells PH levels
the sodium pump as always provides the Na+ gradeint for many of these transporters to work
Acid extruders
Na+/H+ exchanger removes H+ from cell
also regualtes cell volume
inhibited by Amiloride
NBC - the Bicarobonate co transporter - a Na+ dependent Cl-/HCO3- exchanger removes H+ and Cl- from cell by letting Na+ and HCO3- (base) into the cell
an ANTIPORT
this is removes acid and bring in base
Base Extruders -
Anion exchanger - Cl- is pushed into cell to REMOVE HCO3-
Alkali influx
a symport Na+ and 3 HCO3- cotransporter brings in 3 basic bicarb ions with a sodium ion
if the PH drifts away from the set point - the correct transporters will be activated to return to normal - homeostasis
how do we regulate cell volume ?
transport osmotically active ions - Na+ K+ Cl- out of cell
conc of ions high outside of cell so water will flow out (follow) to balance osmotically - remove ions and water and hence cell shrinks
cell swelling - bring in ions and hence water
what are the mechanisms to resist cell swelling
shrinking ?
any transport that pushes out ions - so water out - shrinks
Draw ions into cell so water follows - swells
how does bicarbonate reabsorption in the proximal tubule work ?
bicarb is a good basic PH buffer, so we want to retain it
NaHCO3 is in ionic form in Lumen of GUT
Na+ is pulled into a gut cell by a NHE
the H+ from the NHE combines with HCO3- to form H2CO3
H2CO3 splits into H2O and CO2 via carbonic anhydrase - small non polar - they diffuse across plasma membrane into cell via and equlibirm
its an equlibirum so they recombine in cell to form H2CO3 -by carbonic anhydrase
H2co3 splits into H+ and HCO3-
H+ is used again by NHE - this is the H+ cycle
HCO3- pumped into blood capiliary via an anion exchange for Cl-
a sodium pump pumps Na+ in cell into the blood capiliary
Explain Renal sodium handling
different regions of renal system retain Na2+ using different mechanism
ie in the thick ascending limb - NKCC2 -Na+, K+ , 2Ca2+ moves from lumen into cell
ROMK pumps K+ back into lumen
KCICT pumps Ca2+ and K+ form cell into capillary
CIC - releases Ca2+ into capiliary
sodium pump pumps Na+ from cell to the capillary
loop diuretics block the NKCC2, so Na+ can no longer enter cell and isnt takken back up
