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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.


What can effectors be?

Enzymes or ion channels.