Session 3 Flashcards
What is primary active transport
Driven directly by the energy released by hydrolysis of ATP to ADP
Catalysed by the transporter
What type of transporter is Plasma membrane Ca2+-ATPase (PMCA) and what does it do
Primary active transporter (drives calcium outside cell against conc grad)
What does ATP synthetase do
Uses proton gradient to allow re entry of protons into matrix and drive synthesis of ATP from ADP
Primary active transporter in reverse mode
What is co-transport
More than one type of ion or molecule may be transported on a membrane transporter per reaction cycle
What type of pump is the Na+-K+-ATPase
Anti port (3Na+ out and 2K+ in) Primary active transport P-type ATPase
Alpha sub unit of Sodium Potassium pump
most important- K+ Na+ and ATP binding sites
How much does sodium pump contribute to the resting membrane potential
Very little
What is mainly responsible for membrane potential
K+ diffusion through channels
What is secondary active transport
Driven indirectly by energy released by hydrolysis of ATP to ADP
Dissipation of gradients formed for another ion or substance provides the energy
What drives the transport of the Na+-Ca2+ exchanger
Dissipation of Na+ gradient from sodium potassium pump
Characteristics of primary active transport of Calcium via direct ATP hydrolysis
High affinity, low capacity
Characteristics of secondary active transport of Calcium (dissipation of Na+ gradient drives it)
Low affinity, high capacity, anti port
What drives the Na+-H+ exchanger
Dissipation of Na+ gradient from sodium potassium pump
What drives Na+-Glucose co-transport
Dissipation of Na+ gradient from sodium potassium pump
Symporter, brings in glucose against conc grad
Examples of co transport systems
Na+-K+-ATPase
Na+-Ca2+-exchange
Na+-H+-exchange
Na+-glucose co-transport (small intestine and kidney)
Transporters in cystic fibrosis
Na+ driven transport of Cl-, not possible due to mutated CFTR, Cl- doesn’t pass out of cell so water doesn’t follow
Transporters in diarrhoea
In gut epithelial cell, Protein kinase A activated CFTR so more Cl- transported out so more water follows
Na+-K+-ATPase functions
Forms Na+ and K+ gradients needed for electrical excitability
Drives secondary active transport (control of pH, regulation of cell volume, Calcium, Absorption of Na+ in epithelia, nutrient uptake e.g. glucose)P
high intracellular calcium is
Toxic to cells
Cells signal by
Small changes in intracellular Ca2+
Control of resting Ca2+
Na+-Ca2+-exchanger NCX
PMCA
SERCA
Mitochondria Ca2+ uniporters
What expels Calcium out of cells and brings it into SR/ER
PMCA out, SERCA in NXC out (especially during cell recovery) uniporter into mitochondria (buffer)
Characteristics of PMCA and SERCA
High affinity low capacity
3 types of control of resting calcium concentration
Primary active transport
Secondary active transport
Facilitated transport
NCX activity is
Membrane dependant- depolarised membrane potential reverses mode of operation (Ca2+ in for example in cardiac action potential)
NCX in ventricular myocytes
-90 = NCX Calcium out \+10 = NCX calcium in -90 = NCX calcium out
NCX in ischeamia
Low oxygen, ATP depleted, sodium pump inhibited, Na+ accumulates in depolarised, NCX reverses, Ca++ in which is toxic
Acid extrudes
NHE, NBC
Base extrudes
AE
NHE mechanism
Exchange Na+ for intracellular H+, regulates pH, 1:1 exchange, activated by growth factors, inhibited by amiloride
NBC and AE are
Bicarbonate transporters involved in cell volume regulation
Cell volume regulation
Swell- extrude ions
Shrink- influx ions
