Lecture 14 — Introduction to Adrenomimetics
Definition and purpose
Adrenomimetic (sympathomimetic) drugs produce effects resembling endogenous adrenergic transmitters. They act at adrenergic receptors or influence the transmitter’s life cycle.
Important examples
Albuterol, amphetamine, dobutamine, dopamine, ephedrine, epinephrine, isoproterenol, metaraminol, methoxamine, norepinephrine, phenylephrine and terbutaline.
What determines a drug’s response?
Response depends on alpha-versus-beta receptor selectivity, actions at the receptors present in a tissue, and compensatory baroreflex mechanisms.
Norepinephrine synthesis
Tyrosine enters the neuron and is converted to DOPA by tyrosine hydroxylase, then to dopamine by aromatic L-amino acid decarboxylase. Dopamine enters vesicles and is converted to norepinephrine by dopamine beta-hydroxylase.
Norepinephrine removal
The lecture covers neuronal reuptake with reuse or MAO metabolism, diffusion into circulation, and extraneuronal uptake/metabolism. MAO and COMT are identified as key metabolic enzymes.
Therapeutic applications
The lecture describes maintaining blood pressure, relieving severe acute bronchospasm, and decongesting nasal mucosa by constricting mucosal blood vessels.
Metabolic effects
Adrenergic stimulation can increase lipolysis, hepatic glycogenolysis and potassium uptake into cells. Beta receptors increase insulin secretion, while alpha-2 receptors reduce it; glucose remains the major regulator.
