Membrane Transporters Flashcards
Facilitated Diffusion
Uses no energy. Mlcs that are too large/charged.
Ex: glucose transporter.
Diffuses in and is then phosphorylated into G-6-P so it can’t bind to transporter (trapped).
Insulin triggers cascade so transporter exocytoses and ends up on the membrane. No glucose? no insulin, no trasnporter.
Pumps
Move solute against energy gradient, require energy, can be electrogenic (Na/K) or non-electrogenic (Na/K/2Cl).. non-electrogenic want to balance ion conc.
If electrogenic activity is governed by Vm.
Primary active or secondary active transporters.
Water
Has no pumps, it always moves down the concentration gradient
Primary active
Energy from splitting ATP.
Na/K pump
Inside cells: pump H into organelles (lysosomes etc)
Pump Ca into mem-bound compartments.
Inside mitochondria: special proton pump F1-ATPase. Runs backwards, allowing H leak across membrane and synthesize ATP.
Secondary active
Energy not from ATP hydrolysis, but from secondary source… often the downhill leak of Na into cells (captured and used).
MOST substances pumped this way. Electrogenic can reverse directions. Tap bigger leak to drive smaller pump (ex: Na/Ca exchanger in heart beats)
2 types.
Types of Secondary active?
- ) Co-transport: move diff. solutes in SAME DIRECTION
2. ) Antiport/exchange: move diff solute in DIFF DIRECTION
Na/K pump importance?
All secondary transport mechanisms depend on Na/K pump and therefore ATP is some way!
Calcium transport
There is a large electrochemical gradient for CA across mem (it is furthest ion from equil). Way higher outside. Electrical and conc gradients are inwards.
Eca= +111mV so Ca will always leak in and get PUMPED OUT
Na/Ca exchange pump
In heart it switches direction with each beat.
At rest exchanger runs forward: Ca out (muscle relaxed) na in.
contract: Ca in (muscle contract) and Na out.
Direction of Ca movement is controlled by Vm (when Vm is more negative than -60 the Na leak rules and drives Ca out, when more positive reverse directions).
Digitalis
Foxglove plant extract. Can make heart beat stronger.
It blocks the Na/K pump
(intracell Na increaes, so reduced energy to all Na driven secondary active transporters, including Na/Ca exchanger. So it inhibits this. and Ca gets trapped in cell… get increased cardiac contractility).
Hydrogen ions
Usually pumped OUT by Na/H exchange pump. H binds buffers (so hardly ever free). Eh= -24 (most cells more neg than this… so H will be pumped out).
H must be pumped out as Na leaks in. (secondary active!)
Chloride ions
They are pumped into some cells by secondary active transport.
Na/K/2Cl cotransporter.
So Ecl becomes more positive.
H-K exchanger
Probably non-existent.
Add K and get acidemia, K goes into cells H out.
Add H get hyperkalemia: H into cells K out.
In reality hyperkalemia causes increased K uptake through Na/K pump (not H/K exchanger), this depolarizes the cells by making ek more positive, this affects electrogenic transporters and INHIBITS 3 bicarb/Na from ICF–> ECF, get acidemia (b/c less bicarb outside)
How can you get cells to take up K from the ECF?
Give glucose and insulin or bicarb.
What happens when pK falls?
Vm depolarizes. Very important mechanism in cardiac action potential.