Phenylephrine is a potent alpha agonist.   

However it is not as potent as adrenaline, because it is missing a hydroxyl group from its aromatic ring. The alpha selectivity is once again conferred by the methyl substitution hanging off the amine group.

Because its missing the second hydroxyl group at the phenyl ring, phenylephrine is not a substrate for COMT. Its half-life is thus longer, because only MAO can digest it.




Isoprenaline is a potent nonselective beta agonist.   

This molecule is essentially the same as adrenaline, with the exception of the isopropyl amine substituent. This confers beta-selectivity, but does not aim the molecule specifically at beta-1 or beta-2 receptors.  With this abnormal-looking ethylamine tail, MAO wont touch it, but with COMT alone the halflife is still very brief, only a few minutes.




Salbutamol is a potent beta-2 agonist.   Like isoprenaline, it has a large amine substituent to confer beta-selectivity; it also has a butyl substituent at position 3 of the aromatic ring  which selects for beta-2 receptors. 

The ethylamine tail is even bigger, and there is no normal hydroxyl groups on the amine ring, so neither MAO nor COMT want to metabolise it, and its halflife is about 90 minutes.



Dobutamine is a potent and moderately-selective beta-1 agonist. Its significant beta selectivity is assured by its huge,  monstrously elongated amine substituent group. It is usually present as a racemic mixture; the (+) isomer is a more potent beta-agonist. There is a beta-2 effect as well as a beta-1 effect. MAO cant handle such a weird-looking ethylamine group, but with  such a normal-looking catechol ring COMT makes short work of dobutamine, and its half-life is 2 minutes.

Dobutamine is weird, as it is a partial alpha-agonist, with a higher affinity (25 times greater!)  for the alpha-1 receptors than noradrenaline. That’s the racemic mixture, anyway. (-) and (+) dobutamine both have the same affinity for the alpha-1 receptor, but (+)dobutamine has practically no alpha-agonist activity  (which essentially makes it an antihypertensive alpha-antagonist). (+)dobutamine also has about 7 times the beta-1 agonist effect as compared to (-)dobutamine. The (+)  enantiomer is also a full agonist at the beta-2 receptor.

Confusing? Yes. In summary;

  • Dobutamine is a potent (full) beta-1 agonist
  • Dobutamine is a potent (partial) alpha agonist, which means it acts as an antagonist in situations where there is massive sympathetic overdrive (or co-administration of alpha agonist)
  • Dobutamine is a weak (full) beta-2 agonist


For this sort of really basic stuff, no matter where you look you will find essentially the same information.

I used chapters from "Goodman & Gilman's The Pharmacological Basis of Therapeutics" 11th ed by Brunton et al, and "Basic & Clinical Pharmacology" 11th ed. By Katzung et al.

I also perused Peck and Hill "Pharmacology for Anaesthesia and Intensive care" as well as the notoriously error-prone "Handbook of Pharmacology and Physiology in Anaesthetic Practice" by Stoelting and Hillier. Neither covered this subject in a depth I found satisfying.

Goodman and Gilman's remains a canonical text.