Multisubunit receptors Flashcards
What does atrial naturetic peptide control?
Secreted by heart muscle cell to control blood volume/pressure.
Decreases venous return to the heart
Causes kidney to excrete more water and sodium by relaxing vascular smooth muscle cells.
What second messenger does ANP use?
NO which activates guanylyl cyclase (second haem group has to be activated for full activation)
What sort of receptor is an ANP receptor?
GPCR
Where are acetylcholine receptors usually found?
Muscularskeletal junctions and neurons
Describe M3 acetylcholine receptor action
On smooth muscle cells increases intracellular Ca2+, causing constriction
Vasculature endothelial cells produce NO which diffuses to smooth muscle
How do M3 Ach actions antagonise each other in Smooth muscle cells and vascular endothelial cells?
In endothelial cells, it produces NO, activating guanylate cyclase. cGMP activates PKG which activates MLCP, causing muscle relaxation
On smooth muscle cells, M3 Ach stimulation activates PLC, creating IP3. This releases Ca2+ from ER which activates MLCK and stimulates muscle contraction
Describe NAchR structure
Pentameric
Each subunit spans membrane 4 times
Na+ influx attracted by Asp and Glu residues, depolarising muscle cell area
Describe activation of Transducin G7
Retinal in rhodopsin (G-protein) absorbs a photon
Retinal goes from 11-cis-retinal to all-trans isomer, causing a conformational change in opsin
cGMP phosphodiesterase is activated, sequestering cGMP and closing Na+ and Ca2+ channels.
Hyperpolarisation happens, causing less neurotransmitter to be released and the brain to perceive this as light
What rhodopsin state binds Gαt?
Meta II
How is the Transducin negative feedback cycle maintained?
Closing of cGMP-gated channels leads to a drop in Ca2+
Ca2+ binding proteins bind to guanylyl cyclase, restoring cGMP and opening channels.
Describe adrenergic receptor structure
GPCRs
Ser in the receptors form H-bonds with the adrenaline catechol ring
Asp and Asn form hydrophobic and ionic interactions with the catechol ring
Upon ligand binding, C3 cytosolic loop changes conformation to activate the G-protein
When adrenaline stimulates Gαq, what happens?
PLCβ is activated, converting PIP2 to IP3 and DAG
IP3 releases Ca2+ from the cytosol, inducing smooth muscle contraction
When adrenaline stimulates Gαi, what happens?
Adenylate cyclase is not activated so muscle does not contract
When adrenaline stimulates Gαs what happens?
Adenylate cyclase is activated, so ATP is converted to cAMP, stimulating cardiac muscle contraction and smooth muscle relaxation
Describe a GPCR response
- Ligand binding on TM3 causes a conformational change which affects the G-protein
- Gα-GDP is displaced by Gα-GTP which dissociates from Gβγ
- Effector is activated/inhibited
- Second messenger levels are altered
