Adrenergic Drugs | The Massachusetts General Hospital Handbook of Neurology

Authors: Flaherty, Alice W.; Rost, Natalia S.

Title: Massachusetts General Hospital Handbook of Neurology, The, 2nd Edition

> Table of Contents > Drugs > Adrenergic Drugs

Adrenergic Drugs

A. See also

ICU Drip, p. 172, for indications and dosing.

B. Alpha-receptor agents

Endogenous ligands: Epinephrine (E) and norepinephrine (NE) have roughly equal binding to -receptors. Dopamine (DA) at high doses (>10 g/kg/min) stimulates -receptors (as well as -receptors).
Location of receptors: Mostly postganglionic sympathetic nervous system.
Alpha₁-receptors: Postsynaptic. Cause vasoconstriction, intestinal relaxation and sphincter constriction, increased heart contractile force, arrhythmias, pupillary dilatation.
- Selective agonists: Phenylephrine, etc.
- Selective antagonists: Prazosin, etc. Peripherally acting.
Alpha₂-receptors: Presynaptic and nonneuronal. Cause platelet aggregation, lower insulin secretion; lower NE and acetylcholine release, some vasoconstriction.
- Selective agonists: Clonidine, dexmedetomidine, etc. Centrally acting. Side effects include dry mouth, dizziness, constipation, low BP.
- Selective antagonists: Yohimbine, etc.

C. Beta-receptor agents

Non-selective agents: Isoproterenol is an agonist; propranolol an antagonist, for both ₁- and ₂-receptors. DA at midrange doses (>2 g/kg/min) stimulates -receptors much more than -receptors.
Beta₁-receptors: Cardioselective. Cause increased heart contractile force, HR, AV conduction; renin secretion. E and NE are approximately equipotent.
- Selective agonists: Dobutamine, etc.
- Selective antagonists: Metoprolol (low dose), etc.
Beta₂-receptors: Cause vasodilation and bronchodilation, intestinal relaxation. E is more potent than NE.
- Selective agonists: Albuterol, terbutaline.