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Questions and Answers
What is the effect of stimulating β1 adrenergic receptors?
Which statement correctly describes the action of α2 adrenergic receptors?
What role does choline acetyl-transferase play in the synthesis of acetylcholine?
Which of the following neurotransmitters stimulates both α and β adrenergic receptors, but varies in potency?
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How is acetylcholine released into the synaptic space?
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What substance blocks the transport of acetylcholine into synaptic vesicles?
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What happens to acetylcholine immediately after its release in the synaptic cleft?
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Which receptor is associated with bronchodilation when stimulated?
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What is the first step in the synthesis of noradrenaline?
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Which mechanism primarily regulates the release of noradrenaline in the synaptic cleft?
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How is noradrenaline predominantly released from presynaptic neurons?
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What role does Monoamine oxidase (MAO) play in the metabolism of catecholamines?
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What type of receptor is primarily involved in the contraction of blood vessels?
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What is the primary function of the catecholamine reuptake mechanisms?
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Which enzyme converts DOPA to dopamine in the synthesis of noradrenaline?
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Which uptake mechanism is more selective to noradrenaline?
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Study Notes
Adrenergic Transmission
- Synthesis of Noradrenaline (NA): Begins with tyrosine, converted through several steps involving enzymes like tyrosine hydroxylase, DOPA decarboxylase, and dopamine hydroxylase.
- Adrenaline Synthesis: NA is further converted to adrenaline by phenylethanolamine N-methyl transferase enzyme, primarily in the adrenal medulla.
Storage and Release of Noradrenaline
- NA is stored with ATP in presynaptic vesicles.
- Release: Triggered by calcium influx via voltage-gated calcium channels, leading to exocytosis.
- Non-exocytotic Release: Certain drugs like amphetamine can displace and release NE from vesicles.
Regulation of Noradrenaline Release
- Auto-inhibitory Feedback Mechanism: Release of NA stimulates α2 receptors in the presynaptic neuron, inhibiting further release.
Elimination of Catecholamines
-
Reuptake:
- Uptake 1 (presynaptic): More selective for NA.
- Uptake 2 (extraneuronal): Occurs in effector organs like the heart and smooth muscle; more selective for adrenaline.
-
Metabolism:
- Monoamine Oxidase (MAO): Found in mitochondria, primarily in neurons.
- Catechol-O-Methyl Transferase (COMT): Found in various neuronal and non-neuronal tissues.
Classification of Adrenoceptors
- Divided into two main classes:
- α receptors: (α1 and α2)
- β receptors: (β1, β2, and β3)
Actions of Adrenergic Receptors
-
α1 Receptors:
- Found in smooth muscle of various organs, causing contraction of blood vessels.
- Relaxation of the gastrointestinal tract (GIT).
- Contraction of all sphincters (GIT, urinary).
- Mydriasis (dilation of pupil) due to contraction of the dilator pupillae muscle.
-
α2 Receptors:
- Found in presynaptic neurons, CNS, and blood vessels.
- Inhibit neurotransmitter release.
- Promote platelet aggregation.
- When postsynaptically, they can function similar to α1 receptors.
-
β1 Receptors:
- Primarily found in the heart, increasing contractility and heart rate upon stimulation.
-
β2 Receptors:
- Present in smooth muscle, leading to bronchodilation, peripheral vasodilation, relaxation of visceral smooth muscle, and skeletal muscle tremor.
- Increase aqueous humor secretion.
- Increase liver glycogenolysis.
-
β3 Receptors:
- Role in lipolysis and thermogenesis.
Adrenergic Receptor Agonist Potency
- Adrenaline, noradrenaline, and isoprenaline act on both α and β receptors with varying potencies.
- Noradrenaline more strongly stimulates α receptors.
- Isoprenaline more strongly stimulates β receptors.
Acetylcholine (ACh) Synthesis
- Choline Uptake: Transported from extracellular fluid into the cytoplasm of cholinergic neurons by an energy-dependent carrier system.
- Acetylcholine Synthesis: Choline acetyltransferase catalyzes the reaction of choline with acetyl CoA to form acetylcholine.
Storage of Acetylcholine
- Packaged into presynaptic vesicles via active transport.
- Mature vesicles contain ACh, ATP, and proteoglycans.
- Vesamicol blocks the uptake of ACh into synaptic vesicles.
Release of Acetylcholine
- Action potential arrival at the nerve terminal opens voltage-gated calcium channels, increasing intracellular calcium concentration.
- This triggers fusion of vesicles with the cell membrane, releasing their contents into the synaptic space.
- Botulinum toxin: Blocks the release of ACh.
Degradation and Recycling of Acetylcholine
- Degradation: Acetylcholinesterase (AChE) cleaves ACh into choline and acetate in the synaptic cleft.
- Recycling: Choline is recaptured by a high-affinity uptake system, transported back into the neuron, and used for the synthesis of new acetylcholine.
Acetylcholine Receptors
- Two major classes of receptors in the parasympathetic system:
- Nicotinic receptors:
- Muscarinic receptors:
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Description
This quiz covers the synthesis, storage, release, and regulation of noradrenaline and adrenaline in adrenergic transmission. Key processes including enzyme involvement, auto-inhibitory feedback mechanisms, and catecholamine elimination are explored. Test your understanding of this vital physiological process.
