Flashcards in 13. Effector Mechanisms Deck (13):
What are some examples of enzyme effectors?
Adenylyl cyclase, phospholipase C, phopshoinositide 3-kinase and cGMP phosphodiesterase.
What are some examples of effector ion channels?
Voltage-operated Ca2+ channels (VOCCs) and G protein-regulated inwardly-rectifying K+ channels (GIRKs).
What are the cAMP targets?
cAMP-dependent protein kinase, if cAMP increases, PKA activity increases.
Also Epacs and CNGs.
What are some Gs-coupled receptors involved in regulation of adenylyl cyclase?
B-adrenoceptors, D1-dopamine receptors and H2-histamine receptors.
What are some Gi coupled receptors involved in regulation of adenylyl cyclase?
a2-adrenoceptors, D2 dopamine receptors and u-opioid receptors.
What happens to cyclic AMP-dependent protein kinase (PKA) with increased cAMP concentration?
cAMP binds to the regulatory subunits of PKA and this releases their grip on the catalytic subunits so the C subunits can phosphorylate their targets.
What does phospholipase C catalyse?
The cleavage of PIP2 into IP3 and DAG.
How is phospholipase C action regulated?
By Gq-coupled receptors: a1-adrenoceptors, M1-muscarinic receptors and H1-histamine receptors.
What is the action of IP3?
It acts on IP3 receptors of the endoplasmic reticulum to allow the exit of Ca2+ from the ER into the cytoplasm.
What is the signal pathway with inotropy in the heart?
Blood-borne adrenaline and sympathetically released noradrenaline can interact with ventricular B1-adrenoceptors to increase the force of contraction (positive inotropy). The adrenaline and noradrenaline act as ligands and cause activation of a G protein that increases cAMP activity and causes VOCCs to open, releasing Ca2+ and increasing contractility.
How is vasoconstriction of vasculature controlled?
Noradrenaline is released sympathetically and interact with vascular smooth muscle a1-adrenoceptors to cause vasoconstriction. Parasympathetically released adrenaline interacts with bronchioles smooth muscle M3-us airing receptors to cause bronchoconstriction.
How is neurotransmitter release modulated?
Modulated by pre synaptic G protein-coupled receptors. GBy subunits inhibit specific types of voltage-operated Ca2+ channels and reduce Ca2+ neurotransmitter release.